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, intact and ovariectomized (OVX) female rats were implanted for telemetered blood pressure (BP) recording. A subcutaneous subpressor dose of ANG II was given alone or concurrently with intracerebroventricular (icv) estrogen, ANG-(1-7), an ANG-(1-7)receptor antagonist A-779 or vehicle for one week (Induction). After a one week rest (Delay), a pressor dose of ANG II was given for two weeks (Expression). In males and OVX 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 actually 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 icv 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 up-regulated mRNA expression of RAS antihypertensive components while both central estrogen and ANG-(1-7) down-regulated 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.
- Sex difference
- Blood pressure
- Angiotensin II
- Central Nervous System
- Copyright © 2013, American Journal of Physiology - Heart and Circulatory Physiology