When blood vessels dilate, the flow of blood is increased due to a decrease in vascular resistance. Therefore, dilation of arterial blood vessels (mainly the arterioles) causes a decrease in blood pressure.
Localized tissues increase blood flow in multiple ways, including releasing vasodilators, primarily adenosine, into the local intersitial fluid, which diffuses to capillary beds provoking local vasodilation.
Many physical factors that influence arterial pressure. Each may in turn be influenced by physiological factors such as diet, exercise, disease, drugs or alcohol, stress, and obesity. In practice, each individual's autonomicnervous system responds to and regulates all of these interacting factors so that the actual arterial pressure response varies widely because of both split-second and slow-moving responses of the nervous system and end organs. These responses are very effective in changing the variables and resulting blood pressure from moment to moment.
Vasoconstriction is the narrowing of blood vessels resulting from contraction of the muscular wall of the vessels, particularly the large arteries and small arterioles. Generalized vasoconstriction usually results in an increase in systemic blood pressure, but may also occur in specific tissues, causing a localized reduction in blood flow.
The mechanism that leads to vasoconstriction results from the increased concentration of calcium (Ca2+ ions) and phosphorylated myosin within vascular smooth muscle cells. When stimulated, a signal transduction cascade leads to increased intracellular calcium from the sarcoplasmic reticulum through IP3 mediated calcium release, as well as enhanced calcium entry across the sarcolemma through calcium channels.
The rise in intracellular calcium interacts with calmodulin, which in turn activates myosin light chain kinase. This enzyme is responsible for phosphorylating the light chain of myosin to stimulate cross-bridge cycling. Once elevated, the intracellular calcium concentration is returned to its basal level through a variety of protein pumps and calcium exchanges located on the plasma membrane and sarcoplasmic reticulum. This reduction in calcium removes the stimulus necessary for contraction allowing for a return to baseline.
Endogenous vasoconstrictors include ATP, epinephrine, and angiotensin II.
Vasodilation is the widening of blood vessels resulting from relaxation of smooth muscle cells within the vessel walls, particularly in the large veins, large arteries, and smaller arterioles.
Generalized vasodilation usually results in a decrease in systemic blood pressure, but may also occur in specific tissues causing a localized increase in blood flow.
The primary function of vasodilation is to increase blood flow in the body to tissues that need it most. This is often in response to a localized need for oxygen, but can occur when the tissue in question is not receiving enough glucose, lipids, or other nutrients. Localized tissues increase blood flow by several methods, including the release of vasodilators, primarily adenosine, into the local interstitial fluid, which diffuses to capillary beds provoking local vasodilation. Some physiologists have suggested the lack of oxygen itself causes capillary beds to vasodilate by the smooth muscle hypoxia of the vessels in the region.
As with vasoconstriction, vasodilation is modulated by calcium ion concentration and myosin phosphorylation within vascular smooth muscle cells.
Dephosphorylation by myosin light-chain phosphatase and induction of calcium symporters and antiporters that pump calcium ions out of the intracellular compartment both contribute to smooth muscle cell relaxation and therefore vasodilation. This is accomplished through reuptake of ions into the sarcoplasmic reticulum via exchangers and expulsion across the plasma membrane.
Endogenous vasodilators include arginine and lactic acid.