Role of the Circulating Renin-Angiotensin System in the Pathogenesis of Hypertension in Transgenic Rats, TGR(mREN2)27

Publisher Website
Google Scholar
Abstract
Transgenic rats, termed TGR(mREN2)27, which carry the mouse ren-2d renin gene, develop fulminant hypertension. To elvaluate the role of the circulating renin-angiotensin system (RAS) in hypertension of TGR(mREN2)27, we determined plasma levels of its components and their regulation by ether-stress. Plasma prorenin was elevated in prehypertensive and in adult heterozygous TGR(mREN2)27 (fourtyfold), when compared with Sprague Dawley (SD) controls, whereas plasma renin concentration (PRC) and angiotensin II were not. In SD rats ether anesthesia increased PRC at day (11 a.m.; fivefold), but not at night (11 p.m.). Ether had no effect on PRC in TGR(mREN2)27. In contrast, ether increased plasma corticosterone levels at day and night in both strains to a similar degree. Our data indicate that plasma active renin is not a pathogenetic factor for hypertension in TGR(mREN2)27 and suggest a primary role of circulating prorenin. The lack of stimulation of PRC by ether in TGR(mREN2)27 probably reflects predominant extrarenal origin of renin.