Regulation of cardiac function involves various intrinsic and extrinsic mechanisms. The Frank-Starling mechanism and rate-induced regulation are the principal intrinsic mechanisms that control myocardial contraction.

The autonomic nervous system primarily regulates heart rate. Sympathetic nervous activity increases heart rate, while parasympathetic (vagal) activity decreases heart rate. When both systems are active, the vagal effects usually dominate. The autonomic nervous system modulates myocardial performance by altering the conductance of calcium ions through the cell membrane via the adenylate cyclase system.

Several reflexes regulate heart rate, including baroreceptor, chemoreceptor, pulmonary inflation, atrial receptor (Bainbridge), and ventricular receptor reflexes.

Hormones like epinephrine, adrenocortical steroids, thyroid hormones, insulin, glucagon, and anterior pituitary hormones also regulate myocardial performance. Changes in arterial blood concentrations of oxygen, carbon dioxide, and hydrogen ions directly impact cardiac function and indirectly influence it through the chemoreceptors.

Arterioles, which are resistance vessels, mainly regulate blood flow through downstream capillaries. Neural and humoral stimuli cause contraction and relaxation of the smooth muscle, which constitutes most of the arteriole walls. The sympathetic nervous system primarily regulates blood flow through neural regulation. Sympathetic nerves to blood vessels exhibit tonic activity, and inhibiting the vasoconstrictor center in the medulla reduces peripheral vascular resistance. Stimulation of sympathetic nerves constricts resistance and capacitance vessels (veins). Parasympathetic fibers innervate the head, viscera, and genitalia, but not the skin and muscle.

Autoregulation of blood flow occurs in most tissues. This process maintains a constant blood flow despite changes in perfusion pressure. Autoregulation relies on a myogenic mechanism where increased transmural pressure causes vascular smooth muscle contraction and decreased transmural pressure leads to relaxation.

There is a significant correlation between tissue blood flow and tissue oxygen consumption, suggesting that blood flow is primarily regulated by a metabolic mechanism. When the ratio of oxygen supply to oxygen demand decreases in a tissue, vasodilator metabolites are released, dilating arterioles and enhancing oxygen supply.

Baroreceptors in the internal carotid arteries and aorta are continuously active and regulate blood pressure on a moment-to-moment basis. An increase in arterial pressure stretches these receptors, initiating a reflex that inhibits the medullary vasoconstrictor center and induces vasodilation. Conversely, a decrease in arterial pressure disinhibits the vasoconstrictor center and induces vasoconstriction. The baroreceptors in the internal carotid arteries.
Fig. 18.28 408 SECTION4Berne & Levy Physiology •Fig. 18.28 Schematic Diagram Illustrating Neural Input and Output of the Vasomotor Region (VR). Arrows indicatedirectionofneuralinputandoutput.IX,glossopharyngealnerve;↑PCO2,increasedpartialpressureofcarbondioxide;↓PCO2,increasedPCO2;↑PO2,increasedpartialpressureofoxygen;↓PO2,increasedPO2;SA,sinoatrial;X,vagusnerve.Aortic bodies SA node Sympathetic chain V R Carotid body X X IX ˜ PCO2 ° PO2 ˜ PCO2 ° PO2 ˜ PCO2 ° PO2 1.
Cardiac function is regulated by a number of intrinsic and extrinsic mechanisms. The principal intrinsic mechanisms that regulate myocardial contraction are the Frank-Starling mechanism and rate-induced regulation.
2.
The heart rate is regulated mainly by the autonomic nervous system. Sympathetic nervous activity increases the heart rate, whereas parasympathetic (vagal) activity decreases the heart rate. When both systems are active, the vagal effects usually dominate. The autonomic nervous system regulates myocardial performance mainly by varying the Ca++ conductance of the cell membrane via the adenylate cyclase system.
3.
The reflexes that regulate the heart rate are the baroreceptor, chemoreceptor, pulmonary inflation, atrial receptor (Bainbridge), and ventricular receptor reflexes.
4.
Certain hormones—such as epinephrine, adrenocortical steroids, thyroid hormones, insulin, glucagon, and anterior pituitary hormones—regulate myocardial performance. Changes in the arterial blood concentrations of O2, CO2, and H+ alter cardiac function directly and, through the chemoreceptors, indirectly.
5. The arterioles (resistance vessels) regulate blood flow mainly through their downstream capillaries. Smooth muscle, which makes up most of the walls of arterioles, contracts and relaxes in response to neural and humoral stimuli. Neural regulation of blood flow is almost completely accomplished by the sympathetic nervous system. Sympathetic nerves to blood vessels are tonically active; inhibition of the vasoconstrictor center in the medulla reduces peripheral vascular resistance. Stimulation of the sympathetic nerves constricts the resistance and capacitance (veins) vessels. Parasympathetic fibers innervate the head, viscera, and genitalia; they do not innervate the skin and muscle.
6.
Autoregulation of blood flow occurs in most tissues. This process is characterized by a constant blood flow in the presence of a change in perfusion pressure. Autoregulation is mediated by a myogenic mechanism whereby an increase in transmural pressure elicits a contraction of vascular smooth muscle and a decrease in transmural pressure elicits a relaxation.
7.
The striking parallelism between tissue blood flow and tissue O2 consumption indicates that blood flow is regulated largely by a metabolic mechanism. A decrease in the ratio of O2 supply to O2 demand of a tissue releases vasodilator metabolites that dilate arterioles and thereby enhance the O2 supply.
8.
The baroreceptors in the internal carotid arteries and aorta are tonically active and regulate blood pressure on a moment-to-moment basis. An increase in arterial pressure stretches these receptors to initiate a reflex that inhibits the medullary vasoconstrictor center and induces vasodilation. Conversely, a decrease in arterial pressure disinhibits the vasoconstrictor center and induces vasoconstriction. The baroreceptors in the internal carotid arteries
Fukuda K, Kanazawa H, Aizawa Y, et al. Cardiac innervation and sudden cardiac death. Circ Res. 2015;116:2005.