Vascular renin-angiotensin system in two-kidney, one clip hypertensive rats.

Abstract

TOMIO OKAMURA, MIZUO MIYAZAKI, TADASHI INAGAMI, AND NOBORU TODA SUMMARY The possible role of the renin-angiotensin system in the maintenance of hypertension in two-kidney, one clip hypertensive rats was studied. Plasma renin activity rose rapidly and markedly in association with the elevation of blood pressure and then decreased gradually, although blood pressure remained high. Renin activity in the lung, aorta, and mesenteric artery also increased with the development of hypertension and then decreased in a way similar to that of plasma renin activity at the chronic stage of hypertension. Plasma angiotensin converting enzyme activity did not change significantly until 16 weeks after unilateral renal artery clipping, whereas vascular angiotensin converting enzyme activity significantly increased at the chronic, but not the acute, stage of hypertension. In chronically renal hypertensive rats, 1-sarcosine, 8-isoleucine angiotensin II or enalapril, an angiotensin converting enzyme inhibitor, lowered the blood pressure and enalapril also lowered the angiotensin converting enzyme activity of vascular tissues. The constrictor effect of angiotensin I was greater in isolated arteries from chronically hypertensive rats than in those from age-matched normotensive rats. These results suggest that the vascular renin-angiotensin system plays an important role in the maintenance of two-kidney, one clip hypertension. Elevated vascular angiotensin converting enzyme activity appears to increase local production of angiotensin II, which results in vasoconstriction by acting directly and indirectly through adrenergic nerves on vascular smooth muscle. (Hypertension 8: 560-565, 1986) KEY WORDS * angiotensin converting enzyme • renal hypertension * angiotensin T HE renin-angiotensin (RA) system plays an important role in the regulation of blood pressure and salt-water balance. Although overacceleration of this system was once considered a major cause of hypertension, this view is no longer prevalent because of the existence of hypertension with low levels of plasma renin activity (PRA), as observed in spontaneous hypertension in rats and low renin essential hypertension in humans. Furthermore, the intriguing findings that angiotensin converting enzyme (ACE) inhibitors can effectively relieve low renin hypertension has directed attention to the kallikrein-kinin system 1 and the prostaglandin system, 2 because ACE

Antihypertensive treatment modulates the association between the D/I ACE gene polymorphism and left ventricular hypertrophy: a meta-analysis

“…First, there is mounting evidence that increased ACE gene expression and ACE activity may stimulate the local rate of angiotensin II production [46][47][48][49] and, in turn, may promote cardiac growth. Second, the D variant of the ACE gene may act only under specific conditions, when physiologic or pathophysiologic processes stimulate left ventricular enlargement.…”

Angiotensin II Generation in Mesenteric Arteries in Rats: Effects of Nephrectomy, Deoxycorticosterone and Dexamethasone.

“…It is hypothesized that the system may play a role in the maintenance of vascular tone (Oliver and Siacca, 1984;Zau 1986) and blood pressure regulation (Thurston et al, 1979;Loundon et al, 1983;Okamura et al, 1986) in hypertensive animal models, either directly or indirectly by facilitating sympathetic nerve transmission (Ziogas et al, 1985;Malik et al, 1976).…”

The Role of the Renin-Angiotensin System in Cardiovascular Disease.

“…This release is greatly inhibited by CEI and stimulated by the perfusion with AOGEN or renin (212,213). Angiotensin release and metabolism may be under regulatory influence of /9-adrenergic tone (214) and adenosine (215) and may vary in different models of experimental hypertension (213,216). More than half of ANG I during a single pass through a bloodless perfusion system is converted to ANG II of which about 50% is degraded or taken up (212).…”