The contractile activity of smooth muscle in the walls of arteries, arterioles, venules, and veins is controlled by many mechanisms. Vascular smooth muscle tone is influenced by remote (for example, centrally mediated) control mechanisms, and by local control mechanisms. Remote control mechanisms can be further subdivided into neural control and humoral control. Alterations in arteriolar smooth muscle contraction that result from these influences are responsible for the changes in resistance that determine the distribution of cardiac output. There is a remarkable variation in basal vascular tone and resistance from organ to organ. Renal arterioles, for example, have a very low resting vascular tone and can constrict markedly in response to stimuli such as hypovolaemia, but they have little capacity to dilate. In contrast, arterioles in the skin have a high resting tone and can both dilate and constrict in response to thermo-regulatory stimuli.
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