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Vasodilator pharma

UVa med pharmacology block 3

QuestionAnswer
Amyl nitrate/Nitroglycerin/isosorbide dinitrate Nitrates - tx Angina (of effort, variant, or unstable) - polyesters of nitric/nitrous acid - generate NO using GSH transferase - activates guanylyl cyclase->cGMP->relaxes smooth muscle - short T1/2 2-8mins, inhaled (AN) or sublingual (NG, ID)
What are the effects of nitrates on the vasculature? VSM: veins>arteries>arterioles, -incr venous capacitance/dec ventricular preload, decr filling pressure->reduced CO & heart size -increase vascular compliance/drop in BP @ higher doses -compensatory incr catchol & RAAS secretion -incr coronary blood fl
What are the organ system effects of nitrates other than the vasculature? Smooth muscle relaxation in -Bronchi- helps in pulmonary HTN -GI -GU- used for ED (viagra) relaxes corpora cavernosa allowing erection -cardiac muscle - relieves coronary spasm, improves flow to ischemic myocardium, improves perfusion
What are the other actions of nitrates beyond smooth muscle relaxation? -Reduce platelet aggregation - reduces infarct size -Form methemoglobin from rxn w/hemoglobin - high affinity for CN-, can help tx CN poisoning
What are the toxicities of nitrate use? Reflex tachycardia & increase in contractility decr diastolic perfusion time postural hypertension throbbing headaches Tolerance (reversibly by interruption)
Verapamil Ca channel blocker - phenyalkylamine - tx HTN (all forms), angina (normal & variant), cardiac arrhyth, HF, blocks trans of chemo out of cells - decrease Ca entry via L-type channel- reduces freq of opening->smooth muscle relaxation
Diltiazem Ca channel blocker - benzothiazepine - tx HTN (all forms), angina (normal & variant), cardiac arrhyth, HF - decrease Ca entry via L-type channel- reduces freq of opening->smooth muscle relaxation
Nimodipine/nifedipine/nifedipine sustained-release/isradipine/amlodipine Ca channel blocker - dihydrophyridine (DHP)-tx HTN (all forms), angina (normal & variant), cerebral vasospasm (nimodipine), - decrease Ca entry via L-type channel- reduces freq of opening->smooth muscle relaxation
What are the T1/2's of the DHPs? Nimodipine: 1-2hrs Nifedipine: 2-6 hrs Nifedipine SR/Isradipine: 8-12 hrs Amlodipine: 30-50 hrs
What are the smooth muscle effects of Ca channel blockers? -VSM>>bronchiolar/GI/uterine -arterioles>arteries>veins -blunt AngII & alpha adrenergic vasoconstriction -more effective in constricted than non-constricted vessels
What makes DHPs special in their effects on smooth muscle? Vascular selective Differ in potency in different vascular beds - e.g. nimodipine selective for cerebral BVs
What are the organ system actions of Ca channel blockers? Renal: natriuresis (aff arteriolar vasodilator-> incr GFP/RBF/GFR, decr Na resorption), may worsen proteinuria Cardiac effects -reduce contractility->decr SV, work, BP -decr pacemaker rate in SA node -decr conduction velocity in AV node
What are the toxicities of Ca channel blockers? -Cardiac depression (non-DHPs) -> arrest, bradycardia, AV block, HF -Myocardial ischemia (short acting DHPs) - reflex tachycard, incr risk of MI -HDN, flushing, constipation, perph edema CI's: systolic HF, renal failure (protection inferior to ACEI)
Hydralazine vasodilator - tx severe HTN (w/beta blocker), reduces renal vascular res - mech unknown but binds avidly to vascular tissue - dilates arterioles not veins-> decr PVR, BP + reflex incr in HR - can induce acute rheumatoid state (10% px's), HDN
Minoxidil vasodilator - tx severe hypertension - dilates arterioles not veins-> incr opening of K-ATP channels-> decr PVR/BP, reflex incr in HR - can cause excessive vasodilation & reflex response, topical tx = rogaine (causes hirsutism)
Sodium nitroprusside Vasodilator - tx hypertensive emergencies & severe cardiac failure - dilates arteries & veins - gen's NO & cGMP-> decr PVR, incr venous capacitance-> profound decr in BP - can cause excessive hypotension, toxic due to CN &/or thiocyanate accumulation
What mechanisms for relaxing smooth muscle are related to cAMP? Raise the cAMP levels by: - Activating Gs - Inhibiting cAMP-Phosphodiesterase
What mechanisms for relaxing smooth muscle are related to cGMP? Raise cGMP by: - Nitric Oxide liberation --> Activate soluble Guanylate Cyclase (Nitrates, Nitrites, Nitroprusside) - ANP A/B receptor activation, which encodes a Guanylate Cyclase.
What mechanisms for relaxing smooth muscle are related to Plasma Membrane channels? Calcium Channel blocking Potassium Channel opening
What mechanisms for relaxing smooth muscle are related to hormones? Blockage of vasoconstricting hormone receptors.
What are the short-acting Nitrates? What are their routes of administration? Amyl Nitrate (Inhaled) Nitroglycerin (Sublingual) Because of their routes of administration, they avoid first-pass hepatic metabolism.
What are the important Intermediate-acting Nitrates? Route of admin? Isosorbide Dinitrate (Oral) Nitroglycerine (Buccal, slow release)
What is the important long-acting Nitrate? Nitroglycerin (Transdermal)
What is the mechanism of action of Nitrates? Generate NO --> Activate Guanylyl Cyclase --> cGMP relaxes smooth muscle.
What are the Indirect Compensatory effects of Nitrates? - Increase in Catecholamines in response to drop in BP --> Tachycardia, and Increased Cardiac contractility. - Increased Renin-Angiotensin --> Retention of Na+ and Water.
What is the effect of Nitrates on Cardiac muscle? - Provides relief from coronary spasm (Vasodilation of epicardial coronary arteries) - Improves flow to Ischemic Myocardium (Vasodilation of large collateral vessels) - Improves Subendocardial Perfusion (Decreased left ventricular diastolic pressure)
Tolerance to Nitrates is based on what clinical variable? What is the mechanism? How do you reverse it? Reduced response with continued exposure related to the dose and frequency. It is due to diminished release of NO from Nitrates, due to reduced availability of tissue thiols. Can be reversed by 8-12hrs of interruption a day.
How do Ca Channel blockers affect Arteries? Veins? Bronchioles? Constricted vs. Nonconstricted beds? - Arterioloes > Arteries >> Veins >> Bronchioles & Other Smooth Muscle - More effective in constricted beds (makes sense... it keeps constriction from happening, instead of enhancing direct relaxation like Nitrates do)
What are some therapeutic uses of Ca-Channel Blockers? - HTN - blacks=whites - Angina (Reduce O2 demand by reducing SV, HR, PVR, Wall tension relax Coronaries, decrease vasospasm) - Supraventricular Tachyarrhyth (Non-DHP) - Diastolic HF (Non-DHP) - Cerebral Vasospasm (Nimodipine) - Multidrug Trans (Vera
What is a unique use for Nimodipine? Why is it the only Ca-Blocker used for this? Cerebral Vasospasm, because it has a high affinity for cerebral vasculature.
What is a unique use for Verapamil? Blocks transport of chemotherapeutic agents out of cells via P170 glycoprotein.
Why are only non-DHP drugs used for Cardiac arrhythmias? Because the non-DHP's also block cardiac Ca2+ channels, and cardiac Na+ channels, which decrease HR, contractility, and AV conduction velocity.
What are some toxicities specific to Non-DHP Ca-Channel Blockers (Verapimil and Diltiazem)? Non-DHP's (Remember their effects on Cardiac Ca and Na channels) can cause: - Cardiac Arrest - Bradycardia - AV Block - Heart Failure
What are some toxicities of DHP Ca-Channel Blockers (Nifedipine, Amlodipine, etc.)? Myocardial Ischemia (short acting DHPs), via reflex tachy and increased risk of adverse cardiac events.
What is a very worrisome adverse affect of Hydralazine? 10% of patients can have induced Acute Rheumatoid state (Arthralgia, myalgia, skin rash, Lupus like).
What are the effects of Sodium Nitroprusside? How is it administered? Dilates Arteries AND Veins and is used Intravenously.
Created by: sam.mrosenfeld
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