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Essay On Autonomic Regulation Of The Heart Notes

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Autonomic regulation of the heart mechanisms of contraction
-cardiac muscle is an electrical synctium- intercalated discs- Gap junctions and desmosomes, action potentials propagate through these gap junctions
-action potentials travel down the T tubules which have travel radially, but unlike skeletal muscle travel axially aswell
-During the plateau phase of action potential in ventricles, calcium influx through L type voltage gated calcium channels which is important for excitation-contraction coupling.
-Excitation-contraction coupling- requires Ca influx through L type Ca channels unlike skeletal muscle where there is mechanical coupling- calcium induced calcium release when calcium binds to Ryanodine receptors
-the calcium binds to cardiac isoform of troponin C - TNNC1. The Ca-TNNC1 releases the inhibition of the cardiac isoform of troponin I on actin. The tropomyosin filaments bound to cardiac troponin T to shift away. This allows myosin to interact with the active sites on the Actin ATP fuels cross bridge cycling and thick filaments slide past the thin filaments and generates tension. Relaxtion of the cardiac muscle a) extrusion of calcium into the extracellular fluid
-when the membrane potential returns to more negative values, and the calcium concentration falls
-Na/Ca exchanger which pumps 3 sodium in and one calcium out
-Sarcolemmal calcium pump b) reuptake of calcium from the cytosol by SR
-calcium pump in the sarcoplasmic reticulum.
-unlike skeletal muscle the SR calcium pump is inhibited by phospholamban. When phosphorylated by cyclic dependent protein its ability to inhibit SR calcium pump is lost c) dissociation of calcium from Troponin C
-as calcium concentrations fall, calcium dissociates from troponin C and blocks the actin myosin interactions and causes relaxation. Adrenergic agonists

increase the rate of relaxation by promoting phoshphorylation of troponin I which enhance the dissociation of calcium from troponin C.
-increase in calcium increase the strength of contraction

Sympathetic input to the heart
-post ganglionic fibres of the cardiac nerves release noradrenaline- innervates the SA node, Atria, Ventricles
-right cardiac nerve-more effect on heart rate , left cardiac nerve-more effect on contractility
-at rest the firing rate is less than vagus nerve
-effect: increase Heart rate and contractility
-noradrenaline binds to B1-adrenergic receptors- trimeric G protein dissociates into As and By subunits. The As subunit activates a membrane bound adenylate cyclase and catalyses the conversion of numerous ATP into cAMP- amplification along pathway means the activation of a single adrenoceptor generates a large number of intracellular messenger molecules
- activated Camp-protein kinase A-phosphorylates various proteins Chronotropic effects
-pacemaker cells: cAMP-positive allosteric effect on HCN4 and increases the openstate probability-greater funny current- greater pacemaker current means the threshold is reached quicker-faster rate of contraction-positive chronotropy
-SA node myocytes the increase in Ca current accelerates the SAN reaching threshold generating action potential
-increase in AV node conduction velocity-dromotropic effect - reduces the time lag between SA node and ventricular contraction and in an ECG shortens the PR interval.
-the protein kinase A also phosphorylates delayed rectifier K channels- increases the probability they are open- resulting increase in repolarising outward current leads to the shortening of ventricular action potentials- reduction in action potential duration means more excitations fit into each minute shortens the QT interval- increase chronotropy Ionotropic effects

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