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Compromise of Endogenous Neuropeptide W Production Abrogates the Dipsogenic and Pressor Effects of Angiotensin II in Adult Male Rats
Author(s) -
Pate A. T.,
Yosten G. L. C.,
Samson W. K.
Publication year - 2013
Publication title -
journal of neuroendocrinology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.062
H-Index - 116
eISSN - 1365-2826
pISSN - 0953-8194
DOI - 10.1111/jne.12102
Subject(s) - medicine , endocrinology , corticosterone , hypothalamus , angiotensin ii , thirst , endogeny , prolactin , receptor , chemistry , hormone
Neuropeptide W ( NPW ), an endogenous ligand for the G‐protein coupled receptor GPR 7, is produced in neurones in the rat hypothalamus and brain stem known to be important in the control of food intake and the neuroendocrine response to stress. In previous studies, central administration of NPW during the light phase increased food and water intake and elevated prolactin and corticosterone levels in conscious, unrestrained male rats. In the present study, central administration of small‐interfering RNA (siRNA) reduced NPW levels in the hypothalamus and resulted in a failure of angiotensin II to stimulate water drinking or increase mean arterial pressure. In addition, si RNA ‐treated animals failed to mount a significant prolactin response to immobilisation stress, at the same time as maintaining a normal corticosterone response. These results suggest that endogenous NPW may be a physiologically relevant, downstream mediator of the central actions of angiotensin II to stimulate thirst and increase arterial pressure. In addition, NPW ‐producing neurones appear to participate in the hypothalamic mechanisms controlling prolactin (but not corticosterone) secretion.