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Cardiac pharm

Physiology and Pharmacology

QuestionAnswer
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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