Unlock the secrets of autonomic control over your heart's activity with this comprehensive guide. Delve deep into the intricate mechanisms by which the sympathetic and parasympathetic nervous systems regulate the heart's performance, covering inotropy, chronotropy, dromotropy, and bathmotropy.
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Autonomic Control of Cardiac Activity
The autonomic system is able to control each of the four properties of the heart: inotropy, chronotropy,
dromotropy, bathmotropy. Both the sympathetic and the parasympathetic systems supply the heart: the
parasympathetic mainly SA and AV nodes while it is less extended in the muscles of the atria and
very little in the muscles of the ventricles; the sympathetic completely the opposite.
• The sympathetic nervous system acts through β1 adrenergic receptors: noradrenaline
is released by cardiac nerves; adrenaline is released in the systemic circulation by the adrenal
medulla. Activation of the β1 receptors triggers activation of adenylyl cyclase by GS: cAMP is
produced and exerts some direct effects (on the pacemaker channels) and some through PKA
(phosphorylation of Ca channels and phospholamban).
• The parasympathetic system affects the heart through the vagus nerve: acetylcholine
activates M2 receptors, coupled to Gi/0, that reduce cAMP levels and produce effects
opposite to those of the sympathetic system; in addition, Gi/0 enhances some K currents
and inhibits Ca currents. Parasympathetic effects of the heart occur at the nodes (SAN and
AVN) and the atrial muscle, but not at the ventricular myocardium.
Control of bathmotropy (excitability)
The control of bathmotropy by the autonomic system is exerted through activation of PKA and the
resulting phosphorylation of calcium channels (L-type).
- Catecholamines reduce the threshold for their opening, favor the open state, and increase
conductance; as a result, calcium ions enter more promptly and more intensely during the action
potential. This action is relevant for the excitability of slow fibers, because these cells lack Na+
channels and their action potential depends on Ca2+ currents.
- Acetylcholine has opposite effects, and further reduces excitability through the direct action of Gi/0
on potassium channels (enhancement) and calcium channels (inhibition).
Higher excitability of pacemaker cells (in the SAN) accelerates heart frequency, by lowering the AP
threshold; in AVN cells, the increased Ca current accelerates conduction.
Control of dromotropy (conduction velocity)
Phosphorylation of calcium channels by PKA (enhanced by cathecolamines and reduced by
acetylcholine) affects the intensity of currents during the AP in slow cells.
This changes the speed of membrane depolarization and the surface area of the membrane that is
instantly depolarized by the AP current; the distance at which the AP is directly triggered and can
regenerate changes, and so does the conduction velocity.
The inhibitory effect of the vagus on conduction velocity is further enhanced by the activation of K
channels and inhibition of Ca channels by Gi/0.
The change in conduction velocity is particularly relevant at the AVN, because it modifies the delay
between atrial and ventricular activation.
Control of inotropy (contractility)
The control of inotropy by the sympathetic system is exerted mainly through activation of PKA and the
resulting phosphorylation of calcium channels and phospholamban:
• Calcium channel (L-type) phosphorylation reduces the threshold for their opening, favors the
open state, and increases conductance; as a result, calcium ions enter more promptly and more
intensely during the action potential; this not only increases the amount of calcium available for
the current contraction, but will also increase the amount of calcium that gets stored
in the SR and will be available for the next contractions.
• Phosphorylation of phospholamban switches off its inhibition of SERCA; the latter increases its
activity and stores more effectively Ca2+ in the SR at the end of myocyte contraction.
• This makes it so that a larger fraction of the cytosolic calcium gets stored in the SR, available
for the next contractions, rather than being extruded from the cell; notice that his increased
efficiency in storing Ca2+ also shortens the duration of the contraction (because Ca2+ is
uptaken more readily from the cytoplasm, ending earlier its effects).
The parasympathetic system has an opposed action on atrial but not on ventricular myocytes.
68 Body At Work II
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