this lecture, second in the series of the heart, introduced the finer details of heart contraction and the nervous system's influence over it. the first broad section was about the general components of the action potential mechanism in the hearts. cardiac muscle is introduced as an intermediate between skeletal and smooth muscle, in that it has similarities to both (striations similar to skeletal, cell size similar to smooth). the general mechanism of cardiac muscle contraction and relaxation is then described; induced by the SA and AV nodes, which both produce differently shaped AP curves, and propagating throughout the atriums, ventricles, and purkinje fibers.
the molecular mechanism is described as well: Na+ channels initiate the AP and immediately deactivate. Ca2+ plays a crucial role in promoting a longer during AP and in the actual contraction mechanism. L-type channels have a plateau like permeability curve, representing Ca2+ ions flowing in for a long duration (~150ms), which keeps the AP depolarized for much longer (this is also aided by the decrease in outward K+ flux). inside the cell, Ca+ stimulates further release of intracellular calcium from the sarcoplasmic reticulum, which provides the Ca2+ that is mainly used in the muscle contraction. the actual contraction mechanism is nearly (or completely?) identical to skeletal muscle -- Ca2+ binds to troponin, etc. etc.
the nodes are looked at in further detail. the SA node is the sinoatrial node, which is the primary pacemaker of the heart, because its frequency of depolarization is the fastest. the AV node is a conducting pathway between the atria and ventricles, and is slower due to the relative lack of gap junctions, and this allows the delay in contraction between the atria and ventricles. in the nodes, AP's are initiated by fast T-type Ca2+ channels, which are not affected by Ca2+ blockers, have no long plateau (due to the lack of the slow L-type channels), and spontaneously, autorhythmically depolarize due to the actions of the "funny" Na+ channels, which are activated by hyperpolarization and K+ flux.
finally, we zoom out and look at the overall hierarchy of nervous control over the heart, which starts all the way up in the upper brain structures and trickles down to the autonomic nervous system via the sympathetic and parasympathetic neurons. the main differences between the sympathetic vs. parasympathetic control over the heart are elucidated. the sympathetic preganglionic neurons originate in T1-5 of the spinal cord and innervate the neurons in the autonomic ganglia. the postganglionic neurons project to the heart via the cardiac plexus, stimulating the beta1 receptors on the nodes and myocardium, using NE and E as neurotransmitters. the effect on the SA node is to increase heart rate while the effect on the AV node is to increase conductivity (decrease latency?). the sympathetic innervation also uses second messengers to activate the "funny" Na channels.
the parasympathetic nervous system effect on the heart starts with the preganglionic neurons, which route out to the heart via the cardiac plexus, whatever that is, and the post ganglionic neurons innervate the nodes (but not the myocardium). the receptors used are muscarinic receptors, with ACh as the NT and with plenty of ACh esterase in the receptor areas. the vagus nerve (the name of the parasympathetic nerve), by means of directly opening K+ channels on the SA node, using g-proteins but without any second messengers such as cAMP, thereby allows greater outflow of K+ and therefore a lower membrane potential, and therefore a harder time reaching the threshold potential, thereby reducing the heartrate.
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