BLOOD FLOW REGULATION: LOCAL AND NEUROHUMORAL MECHANISMS
Neurohumoral Mechanisms. The autonomic nervous system and circulating vasoactive factors may override local control mechanisms of blood flow regulation in various circumstances, often in an attempt to maintain
an appropriate level of arterial pressure and sufficient blood flow to the brain and heart. The strength of the neural control of blood flow varies among different vascular beds. It is strong in skin, resting skeletal muscle, kidneys, and viscera. It is weak in heart, brain, and exercising skeletal muscle.
Hyperemia refers to a condition where there is
an increase in blood flow. It may be either "active hyperemia" (related to increased activity of a tissue) or "reactive hyperemia" (following a period of ischemia). "Vasodilator metabolites" produced in proportion to metabolic activity enable blood flow to be matched to the metabolic demand.
Autoregulation is the phenomenon by which certain vascular beds
are able to maintain blood flow nearly constant despite changes in perfusion pressure. Both metabolic and myogenic mechanisms contribute to autoregulation.
"Autoregulation" maintains blood flow constant despite
changes in arterial pressure.
Challenges to blood flow regulation include
changes in metabolic demand, obstruction of blood flow, and changes in perfusion pressure.
Individual tissues and organs have the capacity to locally regulate their own blood flow to meet their metabolic and functional needs. The strength of local regulation varies among different vascular beds. Changes in vascular resistance are mediated by
changes in vascular smooth muscle tone in arterioles. Chronic adjustments can also involve structural changes (e.g., number of blood vessels).
The specific characteristics and relative importance of local vs. neural control differ among various regional circulations. Local control predominates in
coronary and cerebral circulations.
Parasympathetic nervous system. The neurotransmitter acetylcholine
decreases HR (muscarinic cholinergic receptors) and may cause vasodilation (muscarinic cholinergic receptors) in a few specific vascular beds. It has minimal or no influence on TPVR.
Extravascular compression of coronary blood vessels by contraction of the left ventricle increases coronary vascular resistance and
decreases coronary blood flow to left ventricle in systole. As a result, most of the left ventricular coronary perfusion occurs during diastole. Therefore, diastolic aortic pressure is considered the upstream driving pressure for blood flow to left ventricle.
Humoral factors with important cardiovascular actions include
epinephrine, norepinephrine,angiotensin, and vasopressin.
Neural and humoral factors influence coronary vascular resistance primarily through
indirect mechanisms related to changes in cardiac workload and metabolic demand.
Vasodilator metabolites play a key role in
local blood flow regulation.
The cerebral circulation is primarily under
local metabolic control, demonstrates strong autoregulation, and is very sensitive to changes in carbon dioxide in blood.
Regional Circulations. The coronary circulation is regulated primarily by
local metabolic factors. The local mechanisms, including changes in the production of "vasodilator metabolites", normally enable changes in myocardial workload and oxygen consumption to be closely matched by changes in coronary blood flow. Thus, changes in metabolic demand are met by changes in coronary flow. Workload and oxygen consumption of the heart are primarily determined by heart rate, ventricular wall stress, and contractility.
Tissues regulate blood flow to meet
metabolic demand.
Skeletal muscle blood flow at rest is primarily under
neural and myogenic control, but during exercise, there is override of this control due to local release of vasodilator metabolites.
Paracrine factors. Vasodilators include
nitric oxide and prostacyclin.
Neurohumoral Control of Blood Flow Important for
regulation of blood pressure and distribution of blood flow.
Both local and neural control mechanisms regulate
skeletal muscle, renal, and splanchnic blood flow.
Neural control predominates in
skin, and can override local control in resting skeletal muscle, kidneys, and splanchnic region when strongly stimulated. Conversely, local control can override neural control under certain conditions (e.g., in exercising skeletal muscle).
The most important autonomic influence on vascular tone is
sympathetic vasoconstriction mediated through binding of the neurotransmitter norepinephrine to alpha adrenergic receptors on vascular smooth muscle. Sympathetic activity maintains a tonic vasoconstrictor influence on the circulation.
The function of the cutaneous circulation is primarily
thermoregulation. Neural control is more important than local control.
Various paracrine factors (nitric oxide, prostacyclin, serotonin, endothelin, etc.) have vasoactive effects on vascular smooth muscle. Basal release of nitric oxide from endothelium maintains a
tonic vasodilator influence on the circulation.
NO provides
tonic vasodilator tone, thereby influencing arterial pressure at rest. Vasoconstrictors: include endothelin, serotonin, and thromboxane.
The splanchnic circulation is an important determinant of
total peripheral vascular resistance and compliance and is regulated by both local and neural mechanisms. Food intake evokes vasodilation.
Blood flow regulation occurs primarily through changes in
vascular resistance which primarily reflects vascular tone of arterioles. ↑ resistance (R) → ↓ blood flow (Q). ↓R → ↑Q. [Q = (Pi-Po)/R].
Intrinsic local mechanisms and extrinsic neurohumoral mechanisms mediate changes in
vascular resistance.
The primary neurotransmitter norepinephrine and circulating epinephrine cause
vasoconstriction (α receptors) and ↑ HR and myocardial contractility
(β1 receptors)
Epinephrine at low-moderate concentrations can evoke vasodilation
(β2 receptors)
Norepinephrine released from sympathetic nerve terminals provides tonic vasoconstrictor tone, thereby contributing to maintenance of arterial pressure. The sympathetic control of vascular resistance is regionally selective.