Renal Perfusion and the Renal Hemodynamic Response to Blocking the Renin System in Diabetes
Are the Forces Leading to Vasodilation and Vasoconstriction Linked?
- From the Departments of Radiology and Medicine, Brigham and Women’s Hospital and Harvard Medical School, Boston, Massachusetts
Abstract
In three groups of subjects, those with type 2 diabetes and nephropathy, those with type 1 diabetes without nephropathy, and healthy volunteers subjected to short-term hyperglycemia, we observed a counterintuitive relationship. In all three groups, baseline renal plasma flow (RPF) was positively correlated with the RPF response to blocking the renin-angiotensin system (RAS). This seems paradoxical in that an opposite result would have been expected if angiotensin-dependent renal vasoconstriction was responsible for the renal vasodilator response to RAS blockade. This suggests a link between the renal vasodilator response, mediated by nitric oxide (NO), and the activation of the intrarenal RAS. The complex interrelationships between hyperglycemia, insulin, NO, and the RAS may result in phenotypes that indicate varying risk of diabetic nephropathy and underlying genetic polymorphisms.
Footnotes
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Address correspondence and reprint requests to Norman K. Hollenberg, Brigham and Women’s Hospital, 75 Francis St., Boston, MA 02115. E-mail: mlansang{at}partners.org.
Received for publication 2 October 2001 and accepted in revised form 11 February 2002.
N.K.H. has received support from Astra-Zeneca and Bristol-Meyers Squibb.
eNOS, endothelial nitric oxide synthase; l-NAME, NG-nitro-l-arginine methyl ester; l-NMMA, NG-monomethyl-l-arginine; NO, nitric oxide; PRA, plasma renin activity; RAS, renin-angiotensin system; RPF, renal plasma flow.
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