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Physiology and Pharmacology

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Cardiac innervation   Parasympathetic via vagus nerve Sympathetic via postganglionic fibres Somatic afferent fibres Intrinsic cardiac nervous system  
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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  
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Effects of adrenergic stimulation   Mainly on If, Ica and Ik - these control heart rate Increases these to give a faster pacemaker, upstroke and recovery  
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Effects of cholinergic stimulation   Can activate K channels, causing hyperpolarisation Antagonises the sympathetic NS and opens IKACh, reducing heart rate and hyperpolarising membrane potential  
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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  
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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 $  
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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  
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Positive ionotropic effects of sympathetic nerve stimulation   Increase in sympathetic stimulation increases contraction force independently of frank starling effects  
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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  
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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  
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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  
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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  
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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  
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Roles of pharmacological compounds   Muscarinic agonists - bradycardia and vasodilation Muscarinic antagonists - tachycardia Beta adrenoreceptor agonists/antagonists - effects heart rate, conduction velocity and contractility  
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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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