Cardiac pharm Word Scramble
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| Question | Answer |
| Cardiac innervation | Parasympathetic via vagus nerve Sympathetic via postganglionic fibres Somatic afferent fibres Intrinsic cardiac nervous system |
| Effects of innervation on the heart | Sympathetic - faster heart rate, faster conduction velocity, stronger contraction and faster relaxation Parasympathetic - slower heart rate, slower conduction velocity - may innervate ventricles but limited evidence |
| Effects of adrenergic stimulation | Mainly on If, Ica and Ik - these control heart rate Increases these to give a faster pacemaker, upstroke and recovery |
| Effects of cholinergic stimulation | Can activate K channels, causing hyperpolarisation Antagonises the sympathetic NS and opens IKACh, reducing heart rate and hyperpolarising membrane potential |
| Ion channels in SAN pace making | Lack of stabilising Ik - more positive and alterable resting potential Stabilised by IKACh Early pacemaker current - If Late pacemaker current - IcaT Upstroke - IcaL Recovery - Ik |
| Effect of beta receptors | Beta adrenoreceptor agonists and sympathetic nerve stimulation increase pacemaker and upstroke rate and rate of beating Reduced RR interval Steeper phase $ |
| Effect of muscarinic receptors | ACh and parasympathetic nerve stimulation hyperpolarise the membrane potential, decrease pacemaker and upstroke rate and rate of beating Increased RR interval Longer phase 4 |
| Positive ionotropic effects of sympathetic nerve stimulation | Increase in sympathetic stimulation increases contraction force independently of frank starling effects |
| Mechanism of beta adrenoreceptor stimulation | Activates adenyl cyclase - cAMP - PKA Phosphorylates L type calcium channels, phospholamban, Ryr, myofilaments Increases calcium induced calcium release from stores and inhibits PLB thus enhancing calcium reuptake |
| Ionotropic effects of sympathetic nerve stimulation | cAMP dependent PKA increases Ca entry through LCVGC - increased CICR Phosphorylation of PLB increases SERCA activity so more Ca in SR - greater release Kinetics of Ca binding myofilaments altered |
| Evidence that IcaL is altered by PKA | Addition of catalytic subunit of PKA increases IcaL Current blocked by verapamil - must be IcaL Therefore beta 1 activation increases calcium transients and contraction |
| Role of protein phosphatase 2A | Activated by muscarinic receptors via RAC1 Dephosphorylates proteins that PKA phosphorylates A counter balance mechanism E.g. dephosphorylates L type calcium channels, Ryr, PLB, Connexin 43 and NCX |
| Changed in pressure volume loops during exercise | Frank starling mechanism Increase in venous return in exercise increases ventricular stretch This increases stroke volume and cardiac output |
| Roles of pharmacological compounds | Muscarinic agonists - bradycardia and vasodilation Muscarinic antagonists - tachycardia Beta adrenoreceptor agonists/antagonists - effects heart rate, conduction velocity and contractility |
| Targets for inotropic agents | Digitalis inhibits NKX Ca sensitiser alters calcium sensitivity of TnC PDE inhibitors inhibit phosphodiesterase - increase conc of cAMP |
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