Sodium and angiotensin in the pathogenesis of experimental renovascular hypertension

Abstract
The effects of simultaneous angiotensin blockade and Na depletion on the development of one-kidney renovascular hypertension were studied in rats. In Na-replete rats, systolic blood pressure (SBP) increased from 102 .+-. 2 to 153 .+-. 11 mmHg by the 12th day after unilateral nephrectomy and subsequent partial occlusion of the renal artery with a 0.22-mm silver clip. When changes in body fluid volume were minimized by Na restriction in a 2nd group of rats, the increase in SBP from 98 .+-. 4 to 149 .+-. 7 mmHg after clipping was not different from that in Na-replete animals. Inhibition of the angiotensin-converting enzyme with SQ 14,225 D-2-methyl-3-mercaptopropanoyl-L-proline during Na restriction prevented the SBP from increasing above 101 .+-. 3 mmHg by the 12th day after nephrectomy and clipping. Once SQ 14,225 administration was discontinued, SBP rose significantly to 148 .+-. 5 mmHg within 5 days. Previous studies showed that neither Na depletion nor angiotensin blockade alone prevented the development of one-kidney renovascular hypertension; the increase in blood pressure resulting from renal artery constriction and contralateral nephrectomy apparently was prevented by suppression of the renin-angiotensin system and body fluid volume.