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UTSW physio block 1
UTSW school of medicine 2009 physiology class
| Question | Answer |
|---|---|
| Fick's First Law of Diffusion | J= -D*A*delta(c)/delta(x) . D = diffusion coefficient, A = area of membrane, c = concentration difference, x = thickness of membrane |
| effects of molecule size on diffusion | proportional to hydrated diameter. An 8-fold larger molecule has 2-fold greater diffusion rates. For mol. weights up to 1000, size doesn't really matter. |
| diffusion time | diffusion time (msec) = distance^2 * 1/2. To go 1 micron takes 1.2 msec. To go 10 microns takes 50 msec. To go 100 microns takes 5 sec. To go 1 mm takes 10 min. |
| Gas Constant R | change of energy in 1 mole of gas per change of temperature of 1 Kelvin. R = 2 calories/K*mole = 8.3 joules/K*mole |
| isoosmotic solution | ~290 mosmol/L |
| osmotic pressure (P) | P=R*T*delta(osmol/L) . Units of energy/volume = pressure/area. |
| concentration energy | Energy/mole = R*T*ln(C1/C2). C = concentration on 1 or the other (2) side of the membrane. |
| [Na+]i vs. o | 6-12 mM in, 140 mM out (1:15 ratio) |
| [K+]i vs. o | 155 mM in, 4 mM out (35:1 ratio) |
| [Cl-]i vs. o | 4-25 mM in, 120 mM out (1:10 ratio) |
| [HCO3-]i vs. o | 10-20 mM in, 24 mM out |
| [Ca++]i vs. o (free) | 0.1-10 microM in (free) vs. 1.2 mM out (1:10K ratio). pCa in = 5 to 7, pCa out = 2.9. |
| [Ca++]i vs. o (total) | 3 mM in, 10-300 microM out. More total calcium inside the cell but more free calcium outside the cell. |
| converting mL/L to moles/L for gases | divide by 22400 (1 mole gas takes up 22.4 L) |
| components of air | 600 Torr N2 (79%), 160 Torr O2 (20%), 27 Torr CO2 (1%) |
| flux across a membrane | J=Kp*A*delta(C) . J = flux, A = membrane area, delta(C) = concentration difference |
| high membrane permeable substances | O2, CO2, NO, NH3, caffeine, ethanol, barbituates, acetate |
| crenation | the spiky appearance of red blood cells when placed in a hypertonic solution |
| spherocytosis | hemolytic anemia in which the ability of RBC's to withstand hypotonic solution stress is reduced |
| Gibbs-Donnan Equilibrium | bulk negatively charged proteins attract a cation shell which is then surrounded by a water shell. Kprotein/Kbulk = Clbulk/Clprotein. In plasma, proteins behave as if they have double the predicted mosmol/L. |
| Oncotic Pressure | osmotic pressure exerted by proteins in plasma |
| Concentration of protein in plasma | 0.8 mM (oncotic pressure = 22 mmHg instead of the predicted 13.5 mmHg) |
| Hemolysis of RBCs by Nystatin | Nystatin makes RBC's permeable to all small ions. K+ enters, attracted to - charged proteins. Cl- enters to maintain electroneutrality. Water follows high osmolarity -> hemolysis. |
| histamine and oncotic pressure | histamine causes capillary endothelial cells to separate, permitting protein to enter the interstitium -> swelling |
| gap junctions/connexins | mol. weight up to 800 can pass |
| porins | mitochondrial/bacterial. let most small molecules through the outer membrane (not present in the inner membrane) |
| alternating access model | binding site on one side of the transporter open first, then on the other side, alternating in availability. Occurs also in the absence of substrate. |
| uniporters | driven by concentration gradients, work faster when substrate is present |
| antiporters/exchangers | binding sites reorient ONLY when substrates are bound, NOT when binding sites are empty. Can generate huge concentration gradients. transporter is closed on both ends in the intermediate state. |
| P-type Ion Pumps | ATP phosphate binds to intracellular pump. E1 = cytoplasmic binding site open, E2 = extracellular open (ion affinity for intracellular species v. low). |
| Order of events in Na/K pumps | 3 Na+ ions bind intracellularly, ATP hydrolyzed, Na+ occluded, deoccluded extracellularly, released. 2 K+ bind, dephosphorylation, occlusion, K+ binding site deoccluded intracellularly, ATP binds, K+ released. (10 msec) |
| V-type Ion Pumps | related to ATP synthase (mitochondria) w/reverse function. 13 subunits, V0 domain in the membrane, V1 domain in the cytoplasm, located in lysosomes/endosomes/secretory vesicles, acidify lumen w/H+, use ATP but gamma Pi is not covalently attached to pump. |
| plasma membrane-located V-type pumps | intercalated cells of kidney (pump protons into urine, allowing HCO3- resorption), osteoclasts, macrophages, neutrophils, sperm (acidified acrosome helps penetrate egg), some tumor cells |
| ABC-Transporters (ATP-binding cassette transporter genes) | 2 ATP binding domains & 2 TM domains. eg. CFTR, MDR (multi-drug resistance, expressed in tumors). Export toxins/lipids/sterols/ions/small mol's/drugs/proteins outside cell or into organelles. critical for cholesterol/phospholipid transport. |
| Bacterial ABC Transporters | pump sugars, vitamins, metal ions into the cell |
| Order of events for ABC transporters | ATP binds each cassette, conformational change = cavity opens, ligands bound to binding domain travel through the cavity. = POWER STROKE |
| transported by Uniporters | glucose, urea, some aa's, fatty acids |
| transported by Symporters | Na-K-Cl, K-Cl, Na-glucose, Na-aa's, Na-NT's, H-lactate |
| transported by Antiporters | Na/H, Na/Ca, Cl/HCO3 |
| examples of P-type pumps | Na-K, Sarcoplasmic reticulum Ca pump, Plasmalemmal Ca pump, H pumps in yeast/fungi/plants |
| examples of ABC Cassette Pumps | MDR, cholesterol & lipid pumps. (50 kinds in humans) |
| examples of F & V pumps | ATP Synthase (F pump), Vesicular H Pump (V pump) |
| electrical potential | (Volts) = energy(Joules)/charge(Coulombs) = charge(Coulombs)/capacitance(Farads) . V = J/C = C/F |
| rate of change of membrane potential | change in Em over time = dEm/dt = -Im/Cm . rate is directly related to current and inversely related to membrane capacitance |
| Nernst Potential | # ions diffusing in one direction = # diffusing in opposite direction. E = RT/FZ * ln(C-out/C-in) = 60 mV/Z * log(C-out/C-in) |
| specific capacitance | capacitance of membrane per unit area. = 1 microF/cm^2 in all cells |
| diffusion potential | the electrical potential difference that attracts anions and cations together |
| How much energy is released when an ion moves down its electrical gradient across a cell membrane? | Energy/mol = z*F*Em . z = valence, F = Faraday constant, Em = membrane potential of the cell. |
| electrochemical potential difference | delta mu = chemical energy (R*T*ln([in]/[out])) + electrical energy (=x*F*Em) |
| energy released by ion channels | released as heat (~50% of excess energy). ATP hydrolysis creates too much energy + ion movement down gradient generates heat. ion channels generate 5-30% of total heat in the body. |
| membrane current | = 1st derivative of membrane potential |
| whole-cell current | Ik = Gk* (Em - Ek) . for potassium. G = impedance = inverse of resistance. driving force exists when Em-Ek does not = 0. |
| cytotoxic Na+ levels | 15 mM (pathological b/c sodium transporters do not function effectively) |
| Cl- regulation in neurons vs. somatic cells | somatic cells [Cl]in <35mM, neurons [Cl]in = 5mM. Neurons have NT-activated Cl channels that hyperpolarize, so must keep [Cl]i lower. Neurons have K-Cl coporters to do so. |
| cytoplasmic pH regulation | 1. sodium/proton exchanger activated allosterically @ proton binding sites (< pH 6.8), 2. anion exchanger exports bicarbonate for imported Cl -> lowers pH when above pH 7 |
| volume regulation: shrink a swollen cell | activate Cl channels -> K follows -> water follows, or K-Cl coporters |
| volume regulation: swell a shrunken cell | 1. activate Na-K-2Cl coporter -> water follows in, 2. activate Na/H exchangers -> H+ leaves cell -> more HCO3- made -> pH rises -> anion exchangers activated -> NaCl enters cell -> water follows |
| # water molecules/ions entering a cell | 187 water molecules follow each ion |
| extracellular free Ca++ regulation | by kidneys, = 1.3 mM |
| intracellular Ca++ regulation | 1. ATP-driven Ca++ pump, 2. Na/Ca exchanger (small increases in cytoplasmic Na increase intracellular Ca immensely) |
| CFTR | chloride channel, 12 TMD's, 2 NBD's, cytoplasmic regulatory R domain. ABC-like structure. mutation in NBD prevents proper folding & export from Golgi. Only P'ated channels can open (P'ated by cAMP-dpdt kinase) |
| tight junctions | water, cations can pass (usually. sometimes only anions can pass) |
| Sweat generation | Na/K pump on basolateral side generates driving force. Na-K-2Cl coporter brings in Cl. K leaves (basal) via channel & Na pumped out (basal). Cl leaves @ apical side channels. Na enters lumen from interstitia (via tight jxn's). water follows (aquaporins). |
| Sweat salt resorption | K enters @ basolateral Na/K pump, K cycles out via channels. Cell negatively charged = Na enters @ apical side, migrates to basal side = negative charge @ lumen side -> Cl enters cell & migrates to basal side. (CFTR important in both membranes) |
| CFTR & diarrhea | bacterial toxins cause diarrhea by activating adenylate cyclase -> cAMP ->phosphorylation of apical CFTR -> activation & Cl export = Na follows = water follows -> diarrhea |
| pancreas & CFTR | Na/K pump basolateral, K leaves through channel, carbonic anhydrase converts CO2 & H2O to HCO3- & H+, H+ -> lumen via Na/H exchanger, bicarbonate exchanged for Cl. CFTR in apical membrane sends Cl back to lumen (- potential), Na follows via tight jxn's. |
| airways & CFTR | CFTR functions as Cl channel + some other fxn (e.g. regulates Na channels |
| glucose absorption in GI tract | Na/K pump in basal membrane, K cycles back through K channels, Na coported w/glucose thorugh apical membrane, glucose exits @ basal membrane via channels. |
| channel gating vs. permeation | gating = what opens channel (Em, extracellular/cytoplasmic ligands, metabolites), permeation = which ions can pass (physical properties of channel + driving force). All modulation of channels by cell signaling alters open probability [gating]) |
| conductance | change of current per change in Em (Siemens = reciprocal of Ohms) |
| Nernst vs. Reversal potential | Nernst = physiological fact for a specific ion. Reversal = measured potential @ which net current = 0 (flow in == out). Nernst = Reversal ONLY if channel perfectly selective for a particular ion (K channels closest). |
| reversal potential of nonselective cation channels | -20 mV |
| patch clamp | 0.2- 1.0 micron diameter pipette, 1 channel isolated, currents of 0.1 to several pA (6 million charges/sec) |
| reversal potentials (each channel) | K -90, Na +60, Cl -80 to -30 (varies with [Cl]in), Ca +90, nonspecific cation -20 |
| channel selectivity | K & Cl completely selective, Na channels have 10% K, v-gated Ca channels have some K |
| structure of K inward rectifiers | 2 TM subunit, homotetramer, P-loop from extracellular to mid-membrane forms pore. poor conductance @ depolarized potentials, but don't close. K-ATP/K-ACh/IRK/ROMK |
| structure of v-gated K channels | 6 TM domains (2 are similar to inward rectifiers -> form pore, other 4 = for voltage sensor), S4 domain = voltage sensor -> physically moves in response to change in voltage |
| structure of v-gated Na & Ca channels | monomer, 4 repeats similar to 4 K subunits, |
| ENAC channel structure | ="Epithelial Na Channels", heterotetramer, each subunit has 2 TM domains w/large extracellular domain |
| Cl channel structure | "CLC family" (does NOT include CFTR), monomer, 2 sets of 6 homologous TM domains, each 6-subunit domain forms an independently-active pore (in between = regulatory domain) |
| ionotropic channels | 4-5 subunits, heterooligomers, bind multiple NT molecules to open (e.g. glu & ACh or GABA), desensitize, excitatory channels are nonspecific cation, inhibitory are Cl channels |
| selectivity filter in ionotropic channel | ions shed associated water, carbonyl groups of protein bind ions lightly, |
| requirements for voltage-gating | 1. selectivity filter (extracellular side), 2. open & close, 3. modulation by sensor, 4. localized to particular cell regions (do not diffuse in membrane) |
| KATP channels | control secretion of insulin from beta cells. low glucose->low ATP ->KATP channels open->decreases Ca AP frequency = prevents Ca activation of insulin release. |
| electrical time constant Tau | time to get to 66% of steady state. Tau = C/G (capacitance/conductance) |
| major factors limiting speed of electrical responses of long cell processes compared with a wire | 1. far larger numbers of ions must cross in cell vs. wire, 2. cytoplasm is far less conductive, 3. membrane conductance is much higher than the cytoplasm conductance |
| space/length constant | distance @ which charge decreases by 66% along a dendrite (higher value when the membrane resistance is higher = fewer K channels open, OR when the cytoplasmic resistance is lower = wider diameter). = sqrt(Rm/Ra) |
| r(m) vs. r(a) | r(m) = axon membrane resistance (ohm*cm), r(a) = longitudinal resistance of axon cytoplasm (ohm/cm) |
| Total membrane resistance Rm | Rm = r(m) * length/Area = Ohms |
| ROMK channel | K+ inward rectifier, activated by low ATP, controls insulin release in kidney. "Renal Outer Medullary Potassium channel" |
| K(ACh) channel | inward rectifier, activated by ACh, control heart rate & neuronal activity |
| TRP channels | transient receptor potential channels. nonselective cation channels permeable to enough Ca to permit Ca signaling |
| Time of Action Potential | neuron = up to 120 m/sec (2 m/sec when unmyelinated), skeletal muscles = 2-10 msec or longer for slower contraction, cardiac = 250 msec long. |
| channel kinetics | Na channels: instantaneous open/deactivate, inactivation (esp. if held at +20mV for a long time). K channels: 1-4 msec open/deactivate, no inactivation. |
| refractory period | Na channels inactivated + K channels still open. Limits rate of firing. |
| Accommodation | Na channels inactivate at an Em just slightly depolarized, so that it is more difficult to fire |
| Pacemaker neurons | nonspecific cation channels responsible for after-hyperpolarization & repetitive firing. More channels = increased firing frequency. |
| Generator potential | nonspecific cation channels in sensory neurons open -> few action potentials. usually followed by accommodation. |
| KATP channel structure | inward rectifier. homotetramer + 4 CFTR-like (ABC Cassette) SUR (sulfonylurea) subunits. NBS's on K channel & SUR's. ADP activates/ATP deactivates. |
| high length constant | = few channels can change membrane potential over long distances + conduction velocity is high |
| motor unit | single alpha motor neuron + all muscle fibers it innervates (alpha motor neurons innervate 20-100 fibers) |
| terminal motor nerve branches | unmyelinated, Na & K channels for AP, V-gated Ca channels for ACh release |
| Botulinum Toxin | injestion of toxin-> transport to axon terminals, endocytosed, protease eliminates ACh exocytosis machinery. in CNS, blocks inhibitory NT's -> muscle rigidity. death from suffocation. |
| Motorneuron Synaptic Cleft | 50 nm wide, 50-300 vesicles fuse, 10,000 ACh molecules released (more than sufficient for receptor stimulation b/c of AChEsterase), fast diffusion. endplate basement membrane has collagen & anchoring laminins. end plate potential (EPP) due to Na. |
| AChR general | anchored to dystrophin @ top of secondary synaptic fold. Muscle nuclei near endplate make more AChR mRNA due to neuronal cytokine. short half-life (esp. when cross-linked by Ab's). 2 ACh bind 2 alpha subunits to open. nonselective cation, but mostly Na. |
| AChR structure | homopentamer, 4 TM domains, large peripheral pores (3 nm) narrowing @ center to 0.6 nm diameter (double the narrowest part of Na or K channel) |
| Myasthenia gravis pathophysiology | Ab's to AChR inhibit neuromuscular transmission. weakness 1st in eyes, then oropharynx. active stage = years of severe effects, inactive state = fluctuations in symptoms, 15-20 years = fixed muscle atrophy. |
| Myasthenia gravis treatment | AChE inhibitors = difficult to titer, & side effects due to smooth muscle & glands. Immunosuppressants work after 4-8 months, must continue on drugs forever. plasma exchange helps immediately, but lasts short-term. Good before surgery & intermittently. |
| Duchenne Muscular Dystrophy | Xp21, recessive, Dystrophin (usually binds actin & sarcolemma glycoproteins that bind laminin -> prevents membrane rupture during contraction). progressive loss of skeletal muscle fibers. |
| myofibril | organelle attaches to cell membrane, thick (myosin & titin) & thin (actin & nebulin) filaments |
| T-tubules in striated muscle | "transverse tubules", contain L-type Ca channels, arranged in triad @ junction of A & I bands (t-tubule + 2 terminal cisternae), |
| striated muscle contraction | nAChR (ionotropic) -> depolarization -> dihydropyridine receptor (L-type Ca) opens, mechanically linked to ryanodine receptor in SR that releases Ca. Ca binds troponin -> contraction. Ca resequestered by ATPase (terminates contraction). |
| Structure of Dihydropyridine Receptor (N-type Ca Channel) | homotetramer (each w/6 TM domains & 1 P-loop). in striated muscle acts as voltage sensor. in heart & smooth muscle acts as C channel. |
| Striated Muscle Contraction Physio | 1 troponin (binds Ca) per tropomyosin (blocks actin) in thin filaments, ATPase activity precedes muscle force, [Ca] goes from 0.1 to 10 micromolar, troponin reveals actin binding site for myosin. |
| Troponin Structure | (3 subunits) TnC subunit binds Ca, pulls TnI subunit from actin site -> tropomyosin moves into groove, revealing myosin binding site |
| Myosin ATPase activity | ATP binds -> myosin releases actin, ATP hydrolyzed -> myosin head cocks, myosin binds actin, Pi released -> power stroke, ADP released. (myosin dissociation of ADP & Pi much faster in presence of actin) |
| malignant hyperthermia | succinylcholine + volatile anaesthetics, prolong ryanodine R opening, mutation -> muscle rigidity, hypermetabolism, high O2 usage & CO2 production (hypercarbia), hyperthermia, rhabdomyolysis. trtmt= dantrolene (blocks RyanodineR) |
| types of muscle contractions | isometric = fixed muscle length (force proportional to myosin binding to actin), concentric = muscle shortening, eccentric = muscle lengthening, isotonic = tension remains same even though muscle length changes |
| stretch-induced muscle damage | eccentric contraction = stretch TRP channel lets in Ca -> calpain activated -> SR damage, increases P-lipase activity-> cell leaks creatine kinase, mitochondria uptake Ca -> increased ROS's & peroxides, decreased Ca sensitivity, decreased force & tetanus |
| ATP recycling in muscle contraction | creatine phosphate phosphorylates ADP. CrP comes from glucose and fatty acids (generates lactic acid). O2 consumption remains high during recovery to restore cell homeostasis. fatigue = Pi & lactic acid buildup |
| energy for muscle contraction: high to low | PCr (only in striated muscle), ATP, Anaerobic Glycolysis, Carbohydrate Oxidation, Fat Oxidation |
| types of muscle fibers | FG (fast glycolytic/Type IIb) = white, SO (slow oxidative/Type I) = red (myoglobin), FOG (fast oxidative glycolytic/ Type IIa) = lots of mitochnodria & lots of glycogen. all use some oxidation/glycolysis. |
| characteristics of SO motor units | high resistance to fatigue, efficient ATP production, modest tension, slow velocity of contraction. Very small. Antigravity/postural muscles. |
| characteristics of FG motor units | rapid & powerful contractions for short periods of time. Lots of myosin. Rapidly contracting, superficial muscles. |
| muscle force development | SO, FOG, then FG fibers recruited, small distal muscles increase firing rate for large force, large proximal muscles recruit additional motor units |
| McArdle's Syndrome | pain, stiffness, & weakness after brief intense activity. accumulated glycogen in muscle. myophosphorylase deficiency. 2nd wind due to fatty acid & hepatic glucose mobilization. rhabdomyolysis -> myoglobinuria. avoid anaerobic exercise, ingest sucrose. |
| glycogen supercompensation | low carb diet, vigorous exercise, high carbs. only in muscles that were trained. on low carb diet, glycogen decreases then rebounds to double []. |
| resting muscle | ATP binds quickly, but is very slowly hydrolyzed |
| cardiac muscle | striated, but not attached to bone. Cannot be overstretched because of fibrous fascia support |
| maximum muscle force | equivalent to the gravitational pull of the weight. faster velocity of contraction for smaller oppositional weights. single isometric twitch force (less than tetanic force). |
| maximal velocity of contraction | dependent on different forms of myosin. stretch during muscle contraction generates extra force. when it happens quickly, myosin heads caught attached -> extra force for a short period of time |
| striated muscle banding | A band = M line + H band + thick filaments, I band = Z disc + thin filaments |
| muscle fatigue | low pCr, glycogen, glucose. high lactate, H. Inflammation & serum creatine kinase high for 5-6 days. satellite cells differentiate into myoblasts & myotubes to replace damaged fibers. |
| denervation | nerve terminals degenerate, nuclei centralize in muscle fiber, loss of sarcoplasm leading to necrosis w/ adipocyte invasion & scar tissue formation. Group atrophy when no healthy axons. |
| renervation | axonal growth cone connects with previous endplates. initially inactive synapse becomes functional with fxnl differentiation of muscle fiber. collateral sprouting in neurodegen disease. |
| muscle wasting | large muscles waste faster. selective loss in muscles w/abundance of one fiber type. Wasting greatest for leg antigravity muscles, least for hand muscles. Decreased myofibrillar protein & glycolytic/oxidative enzymes. |
| strength training | neural adaptation accounts for immediate muscle hypertrophy (mostly fast-twitch) & muscle enlargement occurs over the longterm. FOG fibers increase specificially in intense body building. |
| endurance training | more and larger mitochondria, more capillaries, high glycogen & glycolytic enzymes, little/no hypertrophy. |
| energy for ATP regeneration in different exercise regimes | CrP for low duration & impact. Glycolysis for moderate duration & impact. O2 for high duration & impact. |
| eccentric contraction muscle damage | sarcolemmal, contracile protein, cytoskeletal, & extracellular matrix damage. Excessive Ca activating protease, calpain & P-lipase. Fatty acid free radicals. Neutrophil, macrophage. |
| aging & muscles | FG motor units shrink & SO fibers grow larger. motor neurons degrade + limited sprouting = fewer motor units. |
| structural protein skeletal muscle disease | Duchenne/Becker (Dystrophin), Limb Girdle (Sarcoglycans), or Severe Congenital (Merosin) muscular dystrophies |
| excitation-contraction coupling skeletal muscle disease | Myasthenia Gravis (AChR), Malignant Hyperthermia (Ryanodine R) |
| Metabolic skeletal muscle disease | McArdle's (Phosphorylase), Tarui's (PFK), Carnitine Palmitoyltransferase deficiency |
| subdivisions of the enteric autonomic system | myenteric = food motility. Submucosal plexus = secretions. Both are motor & sensory. |
| celiac ganglion | inhibits gastric, duodenal & gallbladder digestion, stimulates liver glucose release |
| aorticorenal ganglion | stimulates suprarenal gland epinephrine release |
| superior mesenteric ganglion | vasoconstrits intestinal & rectal vessels |
| inferior mesenteric ganglion | vasoconstriction in intestines, ejaculation, constricts urinary sphincter (pelvic plexus), stimulates orgasm |
| superior cervical ganglion | dilates puil, elevates eyelid, stimulates salivation |
| paravertebral thoracolumbar ganglia | accelerate heartrate, relax airways, piloerection, sweaty palms |
| beta 1 receptor mediation | HEART: SA node & ventricles (increase heart rate & contractility), adipocytes (lipolysis). Epi & NorEpi activate. |
| beta 2 receptor mediation | skeletal muscle (vasodilation), bronchi (dilation), GI (decreased motility), detruser (relaxation), skeletal muscle & liver (glycogenolysis), adipocytes (glycogenolysis) |
| alpha adrenergic receptor mediation | skeletal muscle (vasoconstriction), iris radial muscle (contraction), skin & mucosa (vasoconstriction), lung/tummy/intestine (decreased secretions), ejaculation, hair cell piloerection, sweaty palms, liver glycogenolysis |
| muscarinic channel subtypes coupled to Gq | M1,3,5. activate PLC -> PIP2 cleaved to form IP3 -> Ca release. DAG also formed -> PKC activation. |
| muscarinic channel subtypes coupled to Gi | M2, M4. inhibit adenylyl cyclase |
| nAChR structure | 4 TM domains, heteropentamer: 2 alpha, beta, delta, gamma. ACh binds alpha subunit |
| mAChR structure | 7 TM domains. ACh binds = G protein associates -> G-alpha hydrolyzes ATP -> G protein leaves receptor -> G-alpha separates from beta/gamma ->G-alpha(q) activates PLC or G-alpha(i) inhibits adenylyl cyclase |
| alpha & beta adrenergic receptor G-protein coupling | alpha 1/3/5 adrenergic receptor = Gq coupled (activates PLC). beta 1 & 2 receptors = Gs coupled (activated adenylyl cyclase). |
| pupillary dilation vis-a-vis autonomic control | strong light stimulates mAChR -> circular iris muscle contracts -> pupil constriction. weak lights stimulates NE release for alpha1 receptors -> radial muscle contracts -> pupil dilation. No reciprocal inhibition. |
| alpha & beta adrenergic receptor response to Epi vs. NorEpi | Alpha = slightly more sensitive to Epi. Beta1 = equal sensitivity to both. Beta2 = >>> sensitivity to Epi. |
| skeletal muscle response to sympathetic stimulation | beta2 receptors respond to v. low levels of Epi -> vasodilation. Higher levels of Epi + NorEpi activate alpha receptors -> vasoconstriction. Alpha Dominant! |
| average cardiac stats (70 kg woman) | 5 L/minute cardiac output. 5 L blood volume. 60 bpm heart rate. 80 ml stroke volume. exercise -> 200 bpm HR & CO 20 L/min. (for man, increase amounts by 10%) |
| cardiac output equation | CO = SV x HR [remember: work = force x distance = volume x pressure] |
| blood voume percentages | 85% systemic/10% pulumonary. 80% low pressure/15% high pressure. 65% systemic venous/20% systemic arterial. 5% in heart, 10% in lungs at all times. |
| relationship b/tw pressure, velocity & cross sectional area | slowest velocities @ highest cross sectional areas (summed). Highest pressures at lowest cross sectional area (not summed). |
| Windkessel heart analogy | systole SV -> some forward flow of blood, but much energy stored in elastic large arteries. Systolic elastic recoil of large arteries maintains capillary flow. |
| aging and CV function | arteries & the heart become stiff -> increased speed of arterial pressure waves -> decreased contribution of elastic recoil in diastole |
| LaPlace's Law | Wall Stress = [Pressure*Radius/2*WallThickness] (w = wall thickness). Note that wall stress is the same in the left vs. right ventricle even though left ventricle generates 4x the pressure -- it also has 4x the wall thickness. |
| Why is ventricular contraction better described as auxotonic instead of isotonic? | isotonic = contraction against a constant load. But the backpressure from the aorta increases load during ventricular contraction. auxotonic describes contraction against a spring, which is a better metaphor. |
| limitations of peak isovolumetric pressures | must be higher than pressure needed to open the aortic valve |
| Cardiac Work equation | CW = CO x MAP |
| Cardiac Energy Consumption Equation | CEC = CW + Other Energy Expenditures = ~ Cardiac Oxygen Consumption |
| Cardiac Efficiency Equation | CE = CW/CEC = ~25-35% |
| main determinants of cardiac oxygen consumption | heart contractility, heart rate, wall stress |
| dog heart-lung prep | ventricular volume is controlled, vessels to heart are cannulated |
| isolated perfused heart | vessels cannulated. measure/control venous & arterial pressure |
| isolated superfused muscle | thin strips of papillary/cardiac muscle mounted in an oxygenated bath. contraction frequency controlled by electrical stimulation is muscle undergoes nonspontaneous contraction. |
| cardiac myocyte "cell-attached" patch clamp | digest extracellular matrix of heart w/preoteases. control cytoplasm via pipette. study ion channels & transporters. |
| gap junction uncoupling | occurs when hemichannels not fused, acidic cytoplasm, or overly high [Ca] |
| refractory period of cardiomyocytes | plateau of action potential (absolute refractory period) + relative refractory period (huge shock can cause partial action potentials). RyR inactivates every cycle 1-2 sec (not V-gated ion channels). |
| modulating the magnitude of cardiomyocyte contraction | small delta [Ca] has large effect on contractility. Dihydropiridines block Ca influx -> decreased contractility. Ouabain increases Ca transients -> increased contractility. No effect on skeletal muscle @ dose (decreased sensitivity). |
| Ca regulation in ventricular cardiomyocytes | gap junctions -> K+ influx & depolarization. V-gated Na Channels open. L-type Ca Channels open. Ryanodine R opens in response to high [Ca] -> contraction. repolarization by Na/Ca exchanger. |
| contribution of V-gated Ca channels to Ca needed for contraction | 10-25% (also = % Ca extruded by Na/Ca exchanger) |
| cardiac Na/Ca exchanger | 3 Na for 1 Ca. Brings Ca in at beginning of AP (driven by membrane polarization). Brings Ca out during AP (driven by concentration difference). cytoplasmic Na competes w/Ca, so small increases of cytoplasmic [Na] cause large decrease in [Ca] expulsion. |
| mechanism of heart glycosides | ouabain/strophantidin = steroids inhibit small % of Na/K pumps -> decreased Na gradient slows Na/Ca exchanger -> Ca builds up in cytoplasm to 12 mM. [Na] > 15 mM can = Contracture (failure to relax) & myocyte death. e.g. foxglove. |
| cardiac ischemia & ion gradients | lactic acid builds up inside cardiomyocytes -> Na/H pump activated. Na builds up in cells = can now only move Ca into cell. 'Overload' -> Contracture. |
| mitochondrial Ca sensitivity in cardiomyocytes | 10% of cytoplasmic Ca is taken up by mitochondria (Ca uniporter) & released between heart beats (Ca/Na exchanger). Mt Ca stimulates oxidative phosphorylation. |
| L-type vs. N-type Ca Channels | N-type in skeletal muscle. L-type (open a Long time) in cardiac & smooth muscle. |
| Mechanism of dihydropyridines | inhibit L-type Ca channels specifically. e.g. Nifedipine. concentrations needed to affect heart (negative inotropic effect) = 10x higher than concentrations needed to relax arterial smooth muscle. |
| inotropic/chronotropic/dromotropic/contractility | ino = alters strength of muscle contraction, chrono = alters heart rate, dromo = alters conduction rate. contractility = ability of heart to contract independent of pre/afterload. |
| Mechanism of ryanodine | insecticide from bark of exotic trees. skeletal muscle goes into contracture, but not cardiomyocytes (Na/Ca exchanger works harder to extrude Ca from SR). negative inotropic agent. |
| stiffness of cardiomyocytes | rises steeply past stretched lengths of 2.2 microns/sarcomere. Titan protein linked to Z-bands run entire length of sarcomere between filaments. |
| Frank-Starling Mechanism | with greater preload, the left ventricle end-systolic volume is the same, and peak pressures are somewhat increased. |
| mechanism of cardiac stretch-contractility relationship | stretched cardiomyocyte filaments become more compressed with respect to each other = easier crossbridge formation & Ca binding to Troponin C. |
| Anrepp Effect | Preload OR Afterload increase -> stretch receptors activate (takes 20-60 sec to activate) -> Na & Ca enter cardiomyocytes -> 10-20% increase in Ca transient. |
| large delayed beat | conduction to ventricles occasionally fails. next beat = stronger due to: reserve SR Ca released due to RyR reactivation (extra beat caused by ectopic source of AP) |
| frequency inotropy | when several rapid heart beats occur in sequence, subsequent contractions strongly enhanced b/c Ca entering cytoplasm now 'overload's the SR. |
| Treppe / Bowditch Staircase | myocardial contraction strength increases when frequency of stimulation increases. Due to cytoplasmic Na buildup causing decreased Ca extrusion -> Ca buildup in cell |
| effects of Increased Preload on pressure-volume curve | heart contracts more strongly (Frank-Starling). Same End-Systolic Volume. Slightly higher pressures required for mitral valve closing = shift of isovolumetric ejection phase to the right). |
| effects of Increased Afterload on pressure-volume curve | shift of systolic ejection phase upward (more pressure required before aortic valve opens). Less blood is ejected. |
| effects of Contractility Increase on pressure-volume curve. | = 'vigor' of blood ejection (max. systolic pressure). decreased ESV for positive inotropes, increased ESV for negative inotropes. |
| rate of change of membrane potential | directly related to the total membrane current |
| pacemaker atrial myocytes | -65 mV resting potential, slow AP upstroke. SA node faster than AV. no v-gated Na or leak K channels. V-gated Ca Channels, delayed V-gated K channels, If channels. |
| working atrial myocytes | fast AP upstroke, duration (from upstroke to 80% repolarization) = 100 msec. |
| cardiomyocyte repolarization | cardiomyocytes located on outer wall of heart repolarize faster than cells located on inner wall of heat. |
| ventricular action potentials | 200 msec = 2x 'working' atrial myocytes. v-gated Na channels = fast, inactivate @ plateau, reset @ repolarization. 'delayed' v-gated K channels = slow to open (>100 msec) & close. inward rectifier K stabilize V(rest) (open @ - potentials, close during AP) |
| Purkinje fiber AP | repolarizes quickly to 0 mV, plateaus at 0, then repolarizes to -85 mV. |
| Phases of the cardiac AP | 0. depolarization, 1. brief repolarization, 2. plateau, 3. repolarization, 4. inter-AP interval |
| AP velocities in different heart cells | nodes = 0.05 m/sec, cardiomyocytes = 0.3 m/sec, inter-nodal tracts = 1 m/sec, His-Purkinje cell = 3-5 m/sec |
| ECG | magnitude usually of 1 mV or less. P = atrial depolarization. Q = upper ventricular septum, R = ventricles, S = base of left ventricle, ST segment = uniform depolarization, T = ventricular repolarization. atrial repolarization hidden by QRS. |
| why are both P and Q wave positive deviations when one is de- and the other re-polarization? | The direction of the depolarization is opposite to that of the repolarization. |
| PR interval and QT interval | PR should be < 200 msec or else conduction problem b/tw atria & ventricles. QT = time b/tw ventricle AP & end of ventricular repolarization. |
| Triangle of Einthoven | Lead I (0 degrees) left->right arm. Lead 2 left leg -> right arm. Lead 3 left leg -> left arm. P & T largest in Leads 1 & 2. |
| augmented limb leads | unipolar recording w/single positive lead compared against the sum of the other electrodes (-). Gives greater deflections. aVR, aVL, aVF (a for augmented, right/left/foot) |
| Precordial leads for EKG | V1 right side of sternum, V2 on sternum, V6 axillary line |
| cardiac cell metabolic stress | Ca/Na exchanger activated -> slight inward current -> Ca overload -> Ca-dpdt Ca release. Occurs as 'after-depolarization' (after AP) & can lead to another AP. |
| Phase I repolarization | Ventricular Myocytes & Purkinje cells (due to fast inactivating v-gated K channels) |
| K-Inward Rectifier (cardiac) | in all cardiac cells except the nodes. when blocked by barium, all cardiomyocytes become pacemakers (i.e. all cells have If Ch.) |
| K-ATP channels | most abundant. open during ischemia (low ATP) -> raises K-Nernst & Vrest -> prolonged depolarization -> 'injury current' across heart (when localized region of ischemia). ST elevation. |
| ACh-activated K channels | ONLY IN ATRIA cardiomyocytes. Activated by ACh (vagus nerve). Parasympathetic modulation of heart rate. |
| pacemaker definitions | true = normally generates heart beat. latent = pacemaker capability, located outside SA node (e.g. in AV & Purkinje). ectopic = spontaneous AP generation by other cell (usually due to Na/Ca exchanger) |
| cardiac AP | depolarization (V-gated Na) propagates to t-tubules (near Z-lines). V-gated Ca Ch's + Na/Ca exchanger activated. RyR open & release Ca. Ca sequeseterd in SR & by Na/Ca exchanger & a little by Ca pumps. |
| phospholambin | inhibits SR Ca pumps only when it is phosphorylated by cAMP-dpdt protein kinase. |
| autonomic control of heart rate | vagal ACh innervation primarily to atria. sympathetic innervation (NorEpi) = all over heart. |
| sympathetic (NorEpi) molecular FX | NorEpi @ beta1R: Gs ->adenylyl cyclase makes cAMP-> activates PKA-> 1. P-Ca Ch. increased prob. open. 2. P-lamban -> SR loaded w/extra Ca + faster recovery. 3. P-delayed K Ch's increased prob. open (faster repolarization). requires high ATP. |
| sympathetic physiological FX | increased heart rate, contractility, conduction rate (in pacemakers). Higher plateau potential & longer AP's. decreased recovery time. |
| cardiac alpha receptors | involved in cardiomyocyte growth in the long-term |
| ouabain physiology | less energetically expensive than catecholamines + slows heart rate due to vagal reflex in response to increased cardiac output. |
| ACh molecular FX (innervation to ventricles is very slight) | ACh binds mAChR's -> beta/gamma G-protein subunit binds & activates GIRK channel in atria -> hyperpolarized Vrest = decreased heartrate. Atrial contraction strength decreases (shorter AP's). |
| FX of metabolic state on cardiac contraction | 1. low pH -> lower contractile protein sensitivity to Ca, 2. high K currents (leak), 3. downregulated Ca Ch's, 4. low pH + low ATP -> adenosine released extracellularly -> activates GIRK Ch's on other cells & dilates coronary arteries |
| effects of cAMP in cardiac nodal cells | increases Ca open prob., increases If open prob., more Ca enters cells => Na/Ca exchanger generates inward current. ACh can reverse all FX by blocking adenylyl cyclase (even when administered to ventricles). |
| effects of ACh in 'working atrium' | GIRK Ch. activation -> hyperpolarized Vrest -> shorter AP's & less Ca influx (Ca Ch's close immediately upon repolarization). |
| Carbachol | mimics ACh, not broken down by AChEsterases |
| ventricular phases of heart contraction | 1: filling 2ndary to atrial contraction (ventricle 75% full of blood from previous phases of diastole), 2: isovolumic conctraction, 3: rapid ejection, 4: slow ejection, 5: isovolumic relaxation, 6: rapid filling, 7: slow filling |
| stroke work done by the left atrium & ventricle | in P-V curve, work done by atrium = under LV filling line. Work done by ventricle = inside loop! |
| stroke power | =stroke work/ejection time |
| pressure gradient across a cardiac valve (stenosis) | pressure gradient = 4v^2 |
| methods for measuring heart chamber volume | 1. 2D echocardiography, 2. contrast ventriculography, 3. conductance catheter (impedance inversely proportional to volume), 4. multi-gated image acquisition (radioactive tracer in circulation), 5. MRI |
| measuring CO (Fick's principle) | CO = O2 uptake @ lungs/(arterial O2-Venous O2). |
| indicator-dilution method of determining CO | volume of liquid in beaker = amount dye added/([dye]* (t2-t1)). t2 = time disappearance from tube, t1 = time appearance in tube. |
| measuring stroke volume | 1. Electromagnetic Flowmeter, 2. Doppler Method, 3. WD Echo, 4. multi-gated image acquisition (radioactive tracer in circulation) |
| causes of pathological increases in CO | Beriberi (thiamin deficiency), AV shunt, Hyperthyroidism, Anemia, Anciety, Pregnancy (from highest to lowest) |
| CO related to oxygen consumption | directly related. delta-CO:delta-O2-consumption = 5:1 |
| CO related to end-diastolic volume & venous return | directly related to EDV, inversely related to venous return |
| vascular function curve: delta mean systemic pressure | higher mean systemic pressure (from more blood volume/less venous compliance) shifts curve to the left (lower shifts to the right). CHANGES ONLY VENOUS RETURN CURVE. |
| vascular fxn curve: delta arteriolar resistance | decreased TPR (total peripheral resistance) -> clockwise rotation of venous return curve about msfp point (mean systemic filling pressure). counterclockwise rotation of CO curve around 0 point. CHANGES BOTH CURVES, NOT RIGHT ATRIAL P @ equilibrium point. |
| digitalis FX on vascular fxn curve | positive inotropic effect. rotation of CO curve counterclockwise. No FX on venous return curve. |
| msfp point | mean systemic filling pressure point. @ X intercept of venous return curve. |
| splitting of the 1st heart sound | due to either (1) mitral & triscupid sounds, or (2) when left ventrical isovolumic contraction markedly prolonged (when strength:load ratio decreased due to left heart failure). |
| splitting of the 2nd heart sound | closing of each semilunar valve. physiological splitting = during inspiration. more blood enters right atrium & goes to lungs, but less blood leaves lungs = right ventricle takes more time, left ventricle lates less time. |
| FIXED splitting of the 2nd heart sound | due to atrial or ventricular septal defect ejecting blood from left to right |
| PARADOXICAL or REVERSED splitting of the 2nd heart sound | due to (1) left bundle branch block (right ventricle activated first), (2) depressed left ventricle w/ prolonged isovolumic contraction & ejection |
| 3d heart sound | when ventricular pressure drops precipitously below atrial pressure. sound = sudden rush of blood & low frequency vibration due to relaxed ventricular walls |
| diastolic murmur | caused by (1) stenotic AV valves (constant), (2) aortic/pulmonary insufficiency (decrescendo). bt/w S2 & S1 |
| systolic murmur | caused by (1) stenotic semilunar valve (diamond-shaped, begins w/onset of ejection, doesn't overlap w/heart sounds), or (2) AV insufficiency = regurgitation (constant/pansystolic=holosystolic) |
| Grades of heart murmur | 1. v. faint, 2. faint, 3. moderately loud, 4. very loud, 5. extremely loud w/ only edge of stethoscope on chest, 6. extremely loud w/ stethoscope off chest |
| Continuous murmurs | always present, may shift in intensity. caused by patent ductus arteriosus |
| ECG procedural | 1 mV usually = 10 mm tall, speed = 1 mm/0.04 sec |
| EKG signs of heart block | 1st degree: long PR interval. 2nd degree: long (type I) or normal (type 2) PR interval plus occasional lack of R. 3d degree: P not at all in sync w/R |
| EKG signs of bundle branch blocks | Right bundle: wide QRS w/exaggerated Q-R. Left bundle: wide QRS w/elevated QR. |
| EKG signs of Delta Wave (Wolff-Parkinson-White Syndrome) | Shortened PR interval |
| EKG signs of atrial/ventricular fibrillation | atrial = Irregular R-R interval. Ventricular = scribble appearance (fibrillation) & tachycardia (exaggerated sine wave) |
| Classes of arrhythmias | 1. Abnormal impulse Propagation (reentry/block) OR Generation (node/, 2. Narrow OR Wide complex (= originates above/below Bundle of His), 3. Regular OR Irregular |
| 3 examples of abnormal impulse generation arrhythmias (can lead to triggered activity) | (1) premature ventricular contractions, (2) premature atrial contractions, (3) multifocal atrial tachycardia, (4) Delayed or Early after-depolarizations |
| 3 examples of irregular EKG arrhythmias | atrial fibrillation, multifocal atrial tachycardia, premature atrial contractions |
| rate of spontaneous depolarization of pacemakers in the heart | SA 60-80 bpm, AV 40 bpm, ventricular muscle 30 bpm |
| Conditions for reentry | (1) barrier to normal conduction establishes a new circuit, (2) Unidirectional Block (different refractory period) must be present somewhere in the circuit, (3) slow enough conduction speeds to permit recurring impulse to enact contraction again. |
| Drug therapy goals for reentry trtmt | (1) slow conduction (removes unidirectional block), (2) prolong refractory period (prolongs AP) |
| ischemia vs. infarction | ischemia = insufficiency of oxygen & cells damaged (ST depression). Infarction = lack of oxygen & cells die (ST elevation). |
| types of heart failure (4 stages based on risk/structural disease/symptoms) | (1) SYSTOLIC DYSFUNCTION (e.g. abnormally weak contraction), (2) DIASTOLIC DYSFUNCTION (e.g. "stiff ventricle") |
| factors affecting SV | preload/afterload/contracility |
| PCWP vs. LVEDP | Pulmonary Capillary Wedge Pressure catheter in pulmonary vein (in diastole == pressure in LA & LV). Left Ventricular End Diastolic Pressure = pressure measured directly from the left ventricle @ end-diastole. |
| estimating Afterload | aortic pressure or systemic vascular resistance (SVR) |
| measuring contractility | change in pressure / time |
| factors causing low CO | (1) low preload, (2) high afterload, (3) impaired contractility, (4) low HR |
| FX of renin-antiotensin-aldosterone | Na retention + peripheral vasoconstriction. High Na increases blood volume hence preload (can lead to congestivity). Vasoconstriction increases afterload (adds to ventricular wall stress & cardiac O2 consumption). Increased HR requires more O2. |
| causes of pulmonary oedema | LVEDP (filling pressure) past 25 mmHg exceeds pulmonary capillary oncotic presure |
| Left Ventricular Hypertrophy | temporarily relieves Left ventricular wall stress but increases risk of heart failure & ventricular arrhythmia |
| signs of right heart failure | elevated jugular venous pulsations, edema, ascites (= peritoneal oedema), hepatomegaly |
| signs of left-sided heart failure | rales (clicking/rattling/crackling of lungs), orthopnea (shortness of breath while lying prone), paroxysmal noctural dyspnea (shortness of breath), dyspnea on exertion |
| low CO leads to... | fatigue, exercise intolerance, azotemia (high urea due to low clearance), altered mental status |
| phasic smooth muscles | coupled w/gap junctions = single-unit groups. e.g. GI tract/uterus/ureter/bladder. spontaneous myogenic contraction, AP's, gap jxn's, slow phasic contraction. |
| tonic smooth muscles | uncoupled, multi-unit groups -- neural regulation key to coordination. arrector pili/ciliary muscle/iris/vas deferens/large arteries. neurogenic graded depolarizations w/no gap jxn's. Slow sustained contractions. |
| smooth muscle sarcolemma | Na/K pump, Ca/H ATPase pump, V-gated Ca, V-gated K, extracellular Ca activates contraction. NO T-tubules/V-gated Na channels. IP3 release SR Ca = contraction. cAMP = relaxation. |
| smooth muscle SR | lower Ca capacity than heart/skeletal muscle, located close to sarcolemma. |
| smooth muscle organization | higher actin/tropomyosin: myosin ratio than other muscle. no organized sarcomeres. actin linked to cytoplasmic dense bodies (analogous to Z bands). |
| types of smooth muscle x electrochemical mechanism | (1) Ca action potential (slow), (2) pacemaker depolarizations & Ca AP's, (3) graded changes in membrane potentials in response to NT's/hormones [due to e.g. PKC inhibition of K Ch's causing depoloarization] |
| smooth muscle change in [Ca]i with no change in Em | IP3 binds receptor in SR & then rapidly degraded -> SR Ca release |
| types of smooth-muscle AP's | spike, plateau, slow waves |
| slow wave smooth muscle AP mechanism | Ca-dpdt K channels close when low Ca -> depolarization -> V-gated Ca Ch's open -> 1 or several Ca AP's -> Ca-dpdt K Ch's open |
| smooth muscle actomyosin contractions | ATPase activity & contraction stimulated by: Ca/Calmodulin binding to myosin light chain kinase, which then autophosphorylates -> change in conformation -> myosin head can bind actin. terminated by light chain phosphatase (MLCP). |
| mAChR 1,3,5 activation on smooth muscle | INCREASED MLCK ACTIVATION. Gq -> PKC P'ates CPI-17 which inhibits PP1c "catalytic" subunit of MLCP. Gq also -> Rho Kinase activation -> RhoK P'ates & inhibits "myosin protein targeting" subunit (MYPT1) of MLCP. |
| NO & smooth muscle | NOS makes NO (calmodulin-dpdt). NO diffuses to smooth muscle & activates guanylyl cyclase -> cGMP. cGMP activates kinases whose activity decreases cytoplasmic [Ca] in contracting smooth muscle -> decreased MLCK activity & myosin light chain is de P'ated |
| sustained NorEpi during tonic smooth muscle contraction | alpha adrenergic R activation -> decreased [Ca] & decreased myosin P'ation. [ADP] increases, which inhibits myosin crossbridge cycling to conserve ATP. FORCE IS MAINTAINED. |
| smooth muscle relaxation mechanism | beta adrenergic receptor stimulation -> Gs activates cAMP production -> PKA activation ->->->decreased [Ca} & dilation. |
| mechanisms for erection | nonaroused = penis arteries & arterioles constricted. erection = NO & ACh (parasymp.) -> dilation. more blood = spongy tissue fills and occludes exit veins. PDE5 degrades cGMP to GMP. sympathetics ->arteriolar constriction. |
| NorEpi effects on penis vascular smooth muscle | (phasic) alpha adrenergic R's -> Gq activated. IP3-> Ca release. Ca/Calmodulin activates MLCK -> myosin light chain P'ation. (tonic) Ca-sensitizing pathway: Gq activates RhoA -> Rho Kinase activation -> P'ation of regulatory subunit of myosin light chain. |
| Inhibitors of PDE5 | sildenafil, vardenafil, tadalafil (promote smooth muscle relaxation e.g. erection when proper stimulation is present) |
| Locations of opposing Adrenergic sympathetic & Muscarinic ACh FX | SA node, bronchial muscle & gland, GI motility & secretions, urinary detrusor muscle |
| Why are cardiac AP's longer than neuronal AP's? | fewer K Channels in heart + slower opening stoichiometry |
Created by:
rbxbrown
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