Premium
A switch from GABA inhibition to excitation of vasopressin neurones exacerbates the development of angiotensin II ‐dependent hypertension
Author(s) -
Korpal A. K.,
Han S. Y.,
Schwenke D. O.,
Brown C. H.
Publication year - 2018
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.12564
Subject(s) - vasopressin , medicine , endocrinology , angiotensin ii , vasopressin receptor , vasoconstriction , vasopressin antagonists , baroreflex , blood pressure , antagonist , chemistry , receptor , heart rate
Hypothalamic magnocellular neurones secrete vasopressin into the systemic circulation to maintain blood pressure by increasing renal water reabsorption, as well as by vasoconstriction. When blood pressure rises, baroreflex activation normally inhibits vasopressin neurones via activation of GABA ergic inputs. However, plasma vasopressin levels are paradoxically elevated in several models of hypertension, as well as in some patients with essential hypertension, despite increased blood pressure. We have previously shown that vasopressin neurone activity is increased early in the development of moderate angiotensin II ‐dependent hypertension via blunted baroreflex inhibition of vasopressin neurones. In the present study, we show that antagonism of vasopressin‐induced vasoconstriction slows the development of hypertension and that local administration of a GABA A receptor antagonist inhibits vasopressin neurones during, but not before, the onset of hypertension. Taken together, our data suggest that vasopressin exacerbates the increase in blood pressure evident early in the development hypertension and that blunted baroreflex inhibition of vasopressin neurones is underpinned by an excitatory shift in their response to endogenous GABA signalling.