Estrogen regulation of the brain renin-angiotensin system in protection against
angiotensin II-induced sensitization of hypertension
#MMPMID24858844
Xue B
; Zhang Z
; Beltz TG
; Guo F
; Hay M
; Johnson AK
Am J Physiol Heart Circ Physiol
2014[Jul]; 307
(2
): H191-8
PMID24858844
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This study investigated sex differences in the sensitization of angiotensin (ANG)
II-induced hypertension and the role of central estrogen and ANG-(1-7) in this
process. Male and female rats were implanted for telemetered blood pressure (BP)
recording. A subcutaneous subpressor dose of ANG II was given alone or
concurrently with intracerebroventricular estrogen, ANG-(1-7), an ANG-(1-7)
receptor antagonist A-779 or vehicle for 1 wk (induction). After a 1-wk rest
(delay), a pressor dose of ANG II was given for 2 wk (expression). In males and
ovariectomized females, subpressor ANG II had no sustained effect on BP during
induction, but produced an enhanced hypertensive response to the subsequent
pressor dose of ANG II during expression. Central administration of estrogen or
ANG-(1-7) during induction blocked ANG II-induced sensitization. In intact
females, subpressor ANG II treatment produced a decrease in BP during induction
and delay, and subsequent pressor ANG II treatment given during expression
produced only a slight but significant increase in BP. However, central blockade
of ANG-(1-7) by intracerebroventricular infusion of A-779 during induction
restored the decreased BP observed in females during induction and enhanced the
pressor response to the ANG II treatment during expression. RT-PCR analyses
indicated that estrogen given during induction upregulated mRNA expression of the
renin-angiotensin system (RAS) antihypertensive components, whereas both central
estrogen and ANG-(1-7) downregulated mRNA expression of RAS hypertensive
components in the lamina terminalis. The results indicate that females are
protected from ANG II-induced sensitization through central estrogen and its
regulation of brain RAS.
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