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Stress-induced mesenteric vasoconstriction in rats is mediated by neuropeptide Y Y1 receptors

Stress-induced mesenteric vasoconstriction in rats is mediated by neuropeptide Y Y1 receptors mesenteric blood flow; vascular resistance; renergic; sympathetic nerve activity cold stress; nonad- Y (NPY) is a nonadrenergic cotransmitter that is stored in and released from the sympathetic nerves and the adrenal medulla. Although NPY release usually accompanies release of catecholamines, it is particularly associated with more intense and prolonged sympathoadrenomedullary activation, i.e., during severe stress. NPY exerts multiple actions on the cardiovascular system (for review, see Ref. 25) via its specific receptors, three of which are currently known, Y1, Yz, and Y3 (17). The Y1 receptor appears to predominate in blood vessels and mediates NPY-induced vasoconstriction particularly in small arteries from the cerebral, coronary, and splanchnic vascular beds (2, 6, 18). In all vessels, including the large arteries that may H796 0363-6135/96 $5.00 Copyright o 1996 be more resistant to NPY actions, the peptide potentiates the actions of norepinephrine (NE) and other vasoconstrictors. Reciprocally, preexposure of blood vessels to high levels of catecholamines renders them markedly hypersensitive to NPY (16). Because of these pronounced vascular effects and because elevated plasma NPY levels are found (1, 11, 24), hypertension (14), myocardial ischemia (5), and congestive heart failure (9), NPY has been implicated as a mediator of stress-related vasoconstriction. However, http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png AJP - Heart and Circulatory Physiology The American Physiological Society

Stress-induced mesenteric vasoconstriction in rats is mediated by neuropeptide Y Y1 receptors

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Publisher
The American Physiological Society
Copyright
Copyright © 1996 the American Physiological Society
ISSN
0363-6135
eISSN
1522-1539
Publisher site
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Abstract

mesenteric blood flow; vascular resistance; renergic; sympathetic nerve activity cold stress; nonad- Y (NPY) is a nonadrenergic cotransmitter that is stored in and released from the sympathetic nerves and the adrenal medulla. Although NPY release usually accompanies release of catecholamines, it is particularly associated with more intense and prolonged sympathoadrenomedullary activation, i.e., during severe stress. NPY exerts multiple actions on the cardiovascular system (for review, see Ref. 25) via its specific receptors, three of which are currently known, Y1, Yz, and Y3 (17). The Y1 receptor appears to predominate in blood vessels and mediates NPY-induced vasoconstriction particularly in small arteries from the cerebral, coronary, and splanchnic vascular beds (2, 6, 18). In all vessels, including the large arteries that may H796 0363-6135/96 $5.00 Copyright o 1996 be more resistant to NPY actions, the peptide potentiates the actions of norepinephrine (NE) and other vasoconstrictors. Reciprocally, preexposure of blood vessels to high levels of catecholamines renders them markedly hypersensitive to NPY (16). Because of these pronounced vascular effects and because elevated plasma NPY levels are found (1, 11, 24), hypertension (14), myocardial ischemia (5), and congestive heart failure (9), NPY has been implicated as a mediator of stress-related vasoconstriction. However,

Journal

AJP - Heart and Circulatory Physiology – The American Physiological Society

Published: Feb 1, 1996

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