Renal perfusion and the renal hemodynamic response to blocking the renin system in diabetes: are the forces leading to vasodilation and vasoconstriction linked?
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.
Lansang
M Cecilia
MC
Department of Radiology, Brigham and Women's Hospital and Harvard Medical School, 75 Francis Street, Boston, MA 02115, USA.
Hollenberg
Norman K
NK
D003922:Diabetes Mellitus, Type 1 / Q000235:genetics / Q000503:physiopathology*; D003924:Diabetes Mellitus, Type 2 / Q000235:genetics / Q000503:physiopathology*; D006439:Hemodynamics / Q000502:physiology*; D006801:Humans; D006943:Hyperglycemia / Q000503:physiopathology; D009569:Nitric Oxide / Q000502:physiology; D010477:Perfusion; D011110:Polymorphism, Genetic; D012016:Reference Values; D012079:Renal Circulation / Q000502:physiology*; D012084:Renin-Angiotensin System / Q000502:physiology*; D014661:Vasoconstriction / Q000502:physiology*; D014664:Vasodilation / Q000502:physiology*
D009569:Nitric Oxide