A slow intravenous injection of histamine produces marked vasodilation of the arterioles, capillaries, and venules. This causes a fall in blood pressure whose magnitude depends on the concentration of histamine injected, the degree of baroreceptor reflex compensation, and the extent of histamine-induced release of adrenal catecholamines.Vasodilation of cutaneous blood vessels reddens the skin of the face, while a throbbing headache can result from vasodilation of brain arterioles. Vasodilation is mediated through both H1- and H2-receptors on vascular smooth muscle. Stimulation of H1-receptors produces a rapid and short-lived response, whereas stimulation of H2-receptors produces a more sustained response that is slower in onset. Stimulation of H3-receptors on sympathetic nerve terminals inhibits the release of norepinephrine and its associated vasoconstriction.
Histamine increases the permeability of capillaries and postcapillary vessels, resulting in passage of fluid
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