More Autonomic Control of the Heart
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These are Dr. Schechtman's very own notes for this lecture.
I hope you find them helpful.
3 Autonomic Control of the Heart Heart rate is controlled by the brain Many HR responses are based on feedback from the periphery telling the brain what is going on downstairs. The NTS integrates sensory feedback with influences from higher brain areas sends coordinated action plans to Nucleus Ambiguus and Dorsal Motor Nuc of Vagus, and spinal cord. Most important to heart rate are baroreceptors Baroreflexes Baroreceptors in aortic arch and carotid sinuses; relay info to brain via 9th and 10th cranial nerves Actually respond to stretch rather than pressure, so burst with each systole Increased BP slows HR and reduces BP Chemoreflexes Chemoreceptors respond to hypoxia, hypercapnia, and acidosis of blood. Located in carotid and aortic bodies (adjacent to carotid sinus and aorta), relay info via 9th and 10th Excited by hypoxia or hypercapnia stimulate vagal centers, slowing HR, unless input from lung stretch receptors shows enhanced respiration, which increases HR. Lung Stretch Receptors cause tachycardia Important in asphyxia and respiratory sinus arrhythmia Muscle receptors--muscle activity causes tachycardia (forebrain also involved in exercise response) Somatic Pain causes tachycardia Visceral Pain causes bradycardia Distention of the bladder causes reflex tachycardia Respiratory sinus arrhythmia HR accelerates during inspiration, decelerates during expiration Increased vagal activity during expiration Symp activity is increased during inspiration, but released NE is removed slowly damping out rhythmic effects--So RSA is due almost entirely to oscillations in vagal activity and proportionate to vagal tone Caused by central input from respiratory centers and baroreflexes due to change in thoracic pressure Slower HRV--largely sympathetic, thermoregulatory Diving Response--caused by cold water touching trigeminal receptors of face. Heart rate falls due to vagal inhibition of pacemakers. More pronounced in diving animals, and in combination with peripheral vasoconstriction, allow diving mammals to stay submerged up to 2 hours. Medulla-- NTS contains first synapse for all afferents (baroreceptors, chemoreceptors, lung stretch receptors, muscle work receptors). Relays info to Nuc Ambig and Dorsal Motor nuleus to slow heart, and to ventrolateral medulla, which contains symp preganglionic neurons. Cortex-- Motor areas relay exercise info, which contributes to exercise-dependent tachycardia Emotional states, sexual stimulation, attention, etc. affect heart rate via forebrain Hypothalamus-- Is responsible for organized autonomic responses to emotional states Depressor Area recieves input from NTS activates cardial vagal fibers causing HR slowing Defence Area stimulated by amygdala causes tachycardia by inhibiting baroreceptor traffic to NTS Cardiac muscle contracts in basically the same way as skeletal muscle. Control of myocardial performance--Sympathetic NE interacts with beta-adrenergic receptors on cardiac cell membranes; this reaction activates adenylyl cyclase, which raises intracellular levels of cAMP, activating protein kinases that phosphorylate proteins that activate calcium channels in myocardial cell membranes--This increases Ca++ influx during action potential plateau and more calcium is released from sarcoplasmic reticulum in response to each cardiac excitation, increasing contractile strength Sympathetic activity enhances atrial and ventricular contractility (particularly via left stellate nerves) Control of myocardial performance--Parasympathetic Vagus inhibits atrial myocardium (and to a lesser extent ventricular myocardium) and, AV conduction tissue ACh from vagal endings interacts with muscarinic receptors in cardiac cell membranes, inhibiting adenylyl cyclase, hence decreasing myocardial contractility ACh from vagal endings also inhibits release of NE from neighboring sympathetic terminals Conversely sympathetic nerves inhibit release of ACh from neighboring vagal fibers (via activity of NE and neuropeptide Y)
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