Vascular Wall Renin in Spontaneously Hypertensive Rats: Potential Relevance to Hypertension Maintenance and Antihypertensive Effect of Captopril

• Published in: Hypertension (Dallas, Tex. 1979) Vol. 4; no. 4; pp. 487 - 493
• Main Authors: ASAAD, MAGDI M, ANTONACCIO, MICHAEL J, SLOAN, REBECCA S
• Format: Journal Article
• Language: English
• Published: United States American Heart Association, Inc 01.07.1982
• Subjects: Animals; Blood Pressure - drug effects; Blood Vessels - analysis; Captopril - therapeutic use; Hypertension - blood; Hypertension - drug therapy; Nephrectomy; Proline - analogs & derivatives; Rats; Rats, Inbred Strains; Renin - analysis; Renin - blood
• ISSN: 0194-911X; 1524-4563
• DOI: 10.1161/01.hyp.4.4.487

Relationships among systolic blood pressure (SBP), plasma renin activity (PRA), arterial renin concentrations (ARC), and venous renin concentrations (VRC) were examined in spontaneously hypertensive rats (SHR) and normotensive Wistar-Kyoto (WKY) rats before and after treatment with captopril. The ARC was elevated in SHR relative to WKY whereas VRC was not. Similarly, ARC was related to SBP (r = 0.69, p < 0.01) whereas PRA was not (r = 0.04). Captopril (100 mg/kg daily by mouth for 8 days) decreased blood pressure significantly in both SHR and WKY. PRA as well as ARC and VRC were all increased by captopril. Bilateral nephrectomy virtually eliminated PRA but ARC was not significantly reduced over a 24-hour period. Bilateral nephrectomy also markedly attenuated the acute antihypertensive effects of captopril in SHR; however, a modest effect was still apparent. It is suggested that ARC in SHR, being higher than in WKY, may play a role in the genesis or maintenance of hypertension in this model. Furthermore, the effects of captopril in both intact and nephrectomized SHR may be related to the ability of captopril to inhibit the vascular formation of angiotensin II. Finally, vascular renin is probably not renal in origin and responds to typical feedback inhibition as unmasked by captopril administration. (Hypertension 4:487–493, 1982)