Angiotensin and the renal circulation in hypertension.
Converting-enzyme inhibition, whether teprotide, captopril, or enalapril is used, produces a larger increase in renal blood flow in patients with essential hypertension than in normal subjects when they are on a low-salt diet, a quantitative difference. When studies were performed in individuals on a high-salt diet, normal subjects showed little or no response, whereas a substantial number of patients with essential hypertension displayed an increase in renal blood flow with these agents, a qualitative difference. The individuals that show this potentiated response we now are coming to recognize, have a number of features that suggest a distinct subgroup, the "nonmodulators." Normotensive offspring of hypertensive patients show a directionally similar but smaller renal vascular response to converting-enzyme inhibition. These hypertensive patients also show a blunted natriuresis in response to a sodium loading, which is corrected by converting-enzyme inhibition. Several lines of evidence suggest that the locus of action is intrarenal rather than systemic. Plasma renin activity and plasma angiotensin II concentration are not higher in these subjects, and thus cannot account for their potentiated response to converting-enzyme inhibition. Moreover, the infusion of captopril directly into the renal artery in doses far too low to induce a systemic effect increases renal blood flow specifically in these subjects. They also show a blunted rate of renin suppression after a sodium load, although plasma renin activity falls to the same low level at steady state.(ABSTRACT TRUNCATED AT 250 WORDS)[1]References
- Angiotensin and the renal circulation in hypertension. Hollenberg, N.K., Williams, G.H. Circulation (1988) [Pubmed]
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