Autonomic Control Of The Heart Flashcards
extrinsic influences on heart
. Nerves: most important
. Hormones
. Electrolytes: change cardiac function in terms of electrophysiology
Location of preganglionic cardiac sympathetic neurons
. Intermediolateral cell columns of upper 8 thoracic segments of spinal cord
Neurotransmitter released by postganglionic cardiac sympathetic n. Endings
NE
Cardiac sympathetic nerves are distributed to ___
SA node, AV node, and the atrial and ventricular myocardium
T/F sympathetic innervation of the heart is symmetrical
F, fibers on right side have greater effect on HR, fibers on left have greater effect on contractility
Pathway of preganglionic parasympathetic fibers
. Enter in nucleus ambiguus and dorsal motor nucleus of brain stem
. Exit as R/L vagus nn.
. Fibers distributed to SA node, AV node, and atrial myocardium (lesser extent ventricular myocardium)
T/F parasympathetic innervation to heart is asymmetrical
T, right vagus predominantly SA node w/ effect on HR, left vagus predominantly AV node w/ greater effect on AV node conduction
Neurotransmitter released rom postganglionic parasympathetic n. Endings
ACh
Alpha-1 adrenergic receptors
. Found postsynaptically on vascular smooth muscle of coronary blood vessels
. Present on some myocardial cells
. Signal transduction mediated by membrane phospholipid turnover
. Effects of stimulation are minor
How alpha-1 receptors are mediated by phospholipid turnover?
Products of phospholipid hydrolysis mobilize Ca release from intracellular stores
. Inc. Ca influx through Ca channels
Alpha-2 adrenergic receptors
. Act postsynaptically on coronary vascular smooth muscle to reduce cAMP levels
. Effects on heart stimulation are minor
Beta-adrenergic receptors
. Beta-1 in nodal cells and myocardium
. Beta-2 on coronary vascular smooth muscle cells
. Beta-3 on endothelial cells
. Major effect is inc. HR, contractility, and relaxation
. Mediated mostly by beta-1 receptors
Mechanism of sympathetic nerve activity
. Mediated almost entirely by beta-receptors
. Beta-receptors work to inc. cAMP
. NE binds receptor and stimulates Gs pathway to activate adenylate cyclase to activate PKA which inc. cAMP
Ca channel response to sympathetic stimulation
. L-type Ca Channels more likely to stay open when phosphorylated by cAMP-dependent kinase
. Inc. Ca current that leads to Ca-induced Ca release
. Inc. cytosolic Ca levels in myocardial cells directly and indirectly
Sarcoplasmic reticulum response to sympathetic activity
. Phospholamban is a protein that regulates Ca-ATPase and gets phosphorylate by cAMP-dependent protein kinase
. Phosphorylation results in stimulation of Ca-ATPase
. SR sequesters Ca at a faster rate
. Results in faster rate of relaxation but inc. of SR w/ Ca also makes more Ca available for release in subsequent beats
. Causes more rapid relaxation and inc. in contractility
Contractile protein response from sympathetic activation
. Phosphorylation of Tc reduces Ca sensitivity
.. troponin/tropomyosin complex more likely to remain in position that interferes w/ actin-myosin crossbridges formation
. Contributes to enhances relaxation following beta-adrenergic stimulation
. Effects minor overall compared w/ Ca channels
What parasympathetic receptor is most prominent in cardiac cells
muscarinic -2 subtype
What occurs when parasympathetics activate for cardiac cells?
. Stimulation of M2 receptors inhibits adenylate cyclase to dec. cAMP levels
. Stimulates granulated cyclase to inc. cGMP levels that inhibit inc. in Ca current from cAMP
. Activates ACh-activated K channels in atrial and nodal cells (determines HR but not contractility)
Accentuated antagonism
. Effect of parasympathetic stimulation in ventricle is dependent on background level of sympathetic activity
. Low level sympathetic = effect low
. High level sympathetic = effect pronounced
. Effect of parasympathetic is not as dramatic as sympathetic inc. in contractility
Sympathetic control of HR
. Release of NE inc. HR by inc. slope of pacemaker potential by stimulating beta-1 receptors in SA node leading to cAMP inc. in funny current and L-type Ca current
. Circulating E from adrenal gland has same effect and also regulates HR
Parasympathetic control of HR
. Release of ACh stimulates M-2 receptors leading primarily to opening of ACh-activated K channels
. Dec. slope of pacemaker potential slowing depolarization towards threshold
. Hyperpolarizes max. Diastolic potential which takes membrane potential further from threshold
. Parasympathetic stimulation of SA node inhibits L-type Ca current and funny current contributing to dec. in HR
Autonomic control of AV node
. Sympathetic: inc. AV conduction velocity by inc. upstroke velocity of nodal slow APs
. Parasympathetic: dec. conduction velocity through node by inhibiting upstroke of nodal AP
. Very strong vagal stimulation can block APs from conducting from atria through AV node to ventricles (heat block)
Tonic activity of ANS on heart
. Sympathetic activity normally opposes parasympathetic activity
