Autonomic Cardiac Regulation
| Overview |
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- Any person who has experienced fear or elation knows the capacity of emotions to modulate the rate and intensity of cardiac activity. Beyond these higher neurological processes a large variety of other stimuli, extrinsic to the heart, can regulate the beating of the organ and are largely coordinated by the autonomic nervous system innervation of the heart. Autonomic innervation of the heart, both with sympathetic and parasympathetic fibers, can modulate the frequency with which the heart is activated to beat (Chronotropic Effects) along with the intensity of contraction that electrical activation of the myocardium induces (Inotropic Effects).
- SNS innervation to the heart extends from multiple SNS fibers exiting the spinal cord and generally serves to increases cardiac activity whereas parasympathetic innervation to the heart is largely from the vagus nerve and serves to inhibits cardiac activity. In a resting individual, the heart receives some baseline SNS stimulation which accounts for nearly a third of the resting cardiac output. Further SNS stimulation can nearly double the cardiac output whereas inhibition of SNS innervation and activation of parasympathetic fibers can reduce cardiac pumping to nearly zero.
| Chronotropic Effects |
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- Overview
- Chronotropic Effects of the autonomic nervous system affect the frequency with which the heart is activated and thus modulate the heart rate. The mechanism by which chronotropic regulation is achieved is through modulation of Cardiac Action Potential - Rhythmicity, especially of cardiomyocytes in the SA Node.
- SNS Effects
- SNS stimulation increases the heart rate. To do so, SNS fibers release norepinephrine on beta1 receptors of SA Node cardiomyocytes which increase the conductance of the funny sodium channels. This increases the rate of the "Slow Depolarization Phase" which results in more rapid attainment of the threshold potential for initiating the rhythmic cardiac action potential.
- Parasympathetic Effects
- Parasympathetic stimulation decreases the heart rate. To do so, parasympathetic fibers release acetylcholine which activates M2 Receptors on SA Node cardiomyocytes. M2 Receptor activation not only reduces the conductance of Funny Sodium Channels but also increases conductance of the slow potassium channels. Decreased Funny Sodium Channel conductance reduces Ifunny and thus lengthens the rate of depolarization in the Slow Depolarization Phase. Increased Slow Potassium Channel conductance hyperpolarizes the resting membrane potential and thus increases the membrane potential difference that must be overcome to achieve the threshold potential for rhythmic cardiac action potential initiation. In addition to these effects on the SA Node, Vagal fibers innervate the AV node and can slow cardiac action potential propagation through this key juncture. In special intense situations of parasympathetic activation, conduction of the cardiac action potential through the AV node can become completely blocked, resulting in "Heart Block"
| Inotropic Regulation |
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- Overview
- Inotropic Effects of the autonomic nervous system affect the physical intensity with which cardiomyocytes contract given their electrical stimulation. This manifests macroscopically as a change in the contractility of the myocardium. The mechanism by which inotropic regulation is achieved is through modulation of the Cardiac Action Potential - Cellular Basis.
- SNS Effects
- SNS stimulation of the heart increases cardiac contractility. To do so, SNS fibers release norepinephrine on beta1 receptors on contractile cardiomyocytes. SNS activation increases the amount of calcium released into the cytosol during the "Plateau Phase" of the cardiac action potential. This increased cytosolic calcium enhances cardiac excitation-contraction coupling which in turn increases the tension generated by the cardiomyocyte. Increase tension generation by cardiomyocytes throughout the myocardium manifests macroscopically as an increase in contractility.
- Parasympathetic Effects
- Parasympathetic stimulation of the heart reduces cardiac contractility. To do so, parasympathetic fibers release acetylcholine on M2 receptors on contractile cardiomyocytes. Parasympathetic activation reduces the amount of calcium released into the cytosol during the "Plateau Phase" of the cardiac action potential. In addition, it increases the conductance of the slow potassium channels which shortens the "Plateau Phase" by hastening the initiation of the cardiomyocyte "Rapid Repolarization" Phase. Together, these mechanisms reduce cardiac excitation-contraction coupling which in turn reduces the tension generated by the cardiomyocyte. Reduced tension generation by cardiomyocytes throughout the myocardium manifests macroscopically as a reduction in contractility. It should be pointed out, however, that the effects of parasympathetic stimulation on contractility are relatively weak compared to the capacity of the parasympathetic nervous system to modulate the heart rate.