Increased hypothalamic angiotensin-(1–7) levels in rats with aortic coarctation-induced hypertension

Abstract

Since angiotensin (Ang) (1-7) injected into the brain blocked Ang II pressor actions in rats made hypertensive by aortic coarctation (CH), we examined systemic and tissue angiotensin peptide levels, specifically concentrating on the hypothalamic Ang-(1-7) levels. Plasma, heart and kidney isolated from CH rats showed increased levels of Ang I, Ang II and Ang-(1-7) compared with the normotensive group, with Ang II being the predominant peptide in heart and kidney. In the hypothalamus, equimolar amounts of Ang II and Ang-(1-7) were found in the sham group, whereas only Ang-(1-7) levels increased in CH rats. We conclude that aortic coarctation activates systemic and tissue renin-angiotensin system. The increased central levels of Ang-(1-7) in the CH rats suggest a potential mitigating role of this peptide in central control of the hypertensive process.

Angiotensin-(1–7) in Paraventricular Nucleus Modulates Sympathetic Activity and Cardiac Sympathetic Afferent Reflex in Renovascular Hypertensive Rats

“…It has been reported that blockade of endogenous Ang-(1–7) by microinjection of A-779 into the PVN reduces renal sympathetic tone in normal rats [30]. Ang-(1–7) level in hypothalamus is increased in aortic coarctation-induced hypertensive rats [31]. However, it is not known whether Ang-(1–7) in the PVN is involved in the excessive sympathetic activation and the enhanced CSAR in hypertension.…”

Angiotensin II Regulates Cardiac Hypertrophy via Oxidative Stress but Not Antioxidant Enzyme Activities in Experimental Renovascular Hypertension

“…This primary response occurs as a consequence of reduced renal perfusion and subsequent activation of the renin-angiotensin system during the first week of coarctation (10). Furthermore, we previously showed that cardiac and plasma levels of angiotensin II (Ang II) were increased in this renovascular model of hypertension (11), and several studies have demonstrated that aortic coarctation in rats caused cardiac hypertrophy at 2, 6, and 28 days after ligation of the abdominal aorta (12,13).…”

Heme Oxygenase-1 Overexpression Fails to Attenuate Hypertension when the Nitric Oxide Synthase System Is Not Fully Operative

“…Aortic coarctation is a renovascular model of hypertension that depends on angiotensin II function [46] . In this model, we previously showed a redox imbalance in the aorta [9] , heart [8] and kidney [21] and oxidative stress generation that contributed in the development of the hypertensive stage.…”