ENHANCED RENAL SENSITIVITY TO ANGIOTENSIN ACTIONS IN DIABETES-MELLITUS IN THE RAT

The renin-angiotensin system (RAS) has been implicated in the pathogen esis of diabetic nephropathy. In diabetes, renal RAS components are dy sregulated, potentially increasing renal RAS effects. To explore the r enal RAS, studies were conducted in control and diabetic rats. In both groups, intravenous angiotensin (ANG) I and ANG II produced similar i ncreases in mean arterial pressure (MAP). In contrast, glomerular filt ration rate declined only in diabetic rats. Renal plasma flow fell in both groups but decreased more in diabetic rats. Additional groups wer e given the same dose of ANG I directly into the left renal artery, an d hemodynamics were studied in the treated and untreated kidneys. In c ontrast to the intravenous studies, intra-arterial ANG I had no effect on MAP in either group. The renal hemodynamic effects were similar to those in intravenous studies. Additionally, diabetic rats exhibited e nhanced hemodynamic sensitivity in the untreated kidney, suggesting th at renal effects could occur at nonpressor concentrations of circulati ng ANG II. Thus renal (but not systemic) responsiveness to angiotensin s is enhanced in diabetic rats.