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Lecture 6

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Department
Physiology
Course
PHSL232
Professor
Regis Lamberts
Semester
Spring

Description
Extrinsic Control of Cardiac Function Objectives:  Nervous and hormonal control of cardiac function by sympathetic stimulation  Sympathetic and parasympathetic action on excitation (SA node) and its intracellular signalling  Sympathetic action on excitation-contraction coupling (cardiomyocytes) and its intracellular signalling  Sympathetic action on contractility and Frank Starling Curve  Extrinsic Control of contraction by positive inotropic factors, such as glycosides Extrinsic Control:  Noradrenaline: sympathetic nerve terminals: medulla  sympathetic ganglion  electrical and muscle cells  Acetylcholine: released from parasympathetic nerve terminals (of the vagus nerve)  Alter function without a primary change in EDV Autonomic control:  Fight, flight, feeding, fornication Effect of Para/sympathetic nervous systems on the heart:  Controlled by frequency of SA Aps normally 100/min  Change in rate of SA node discharge through autonomic nervous activity  Parasympathetic fibres (vagus nerve)  Sympathetic nerve fibres (cardiac nerves) Excitation: 3 phases:  Pacemaker or pre-potential (Phase 4)  Resting membrane potential is -60/-70mV  Unstable due to funny Na channels: slow influx of Na  T-type calcium channels: influx of Ca  Threshold reached at -50/-40mV  Upstroke (Phase 0)  Voltage operated Ca channels open: Ca influx  Repolarisation (Phase 3) slow K efflux Sympathetic stimulation:  Makes membrane potential less negative: closer to threshold  Faster spontaneous depolarisation: increased slope of pre-potential: reaches threshold sooner  Noradrenaline acts on Beta-Adrenergic receptors  Spontaneous rate of SA node depolarisation is increased: heart rate increases- tachycardia  Intracellular signalling:  Ach binds to M2 muscarinic receptor  G protein  rise in cAMP  Directly increases funny Na current- opens funny channels  PKA phosphorylates Ca handling protein: more T-type Ca: increased Ca concentration  Opening of channels is faster  faster depolarisation  if re uptake is not sped up also, repolarisation will not be sped up therefore HR overall will not speed up.  Rectifier K channels, increasing repolarising K current, shortens duration of the AP Parasympathetic stimulation:  Acetylcholine  muscarinic receptors open K channels  Lowers membrane potential: further away from threshold  Slope of pre-potential is reduced- takes longer to reach threshold  Spontaneous rate of SA node depolarisation is decreased  Decreased HR = bradycardia  Intracellular sign
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