Renin regulation in type II diabetes mellitus: Influence of dietary sodium

Abstract

Numerous abnormalities in the renin-angiotensin system have been described in diabetes mellitus. Plasma renin activity (PRA) has been noted to be low, normal, and high in diabetic patients; these variable results may be explained by differences in patient selection and standardization of study conditions. We evaluated PRA and inactive renin responses in Type II normotensive (n=7) and hypertensive (n=12) diabetic patients specifically selected for no or minimal evidence (background retinopathy) for microvascular complications. Patients were studied in a metabolic ward after 7 days on a constant low sodium (20 meq/day) and 7 days on a high sodium (250 meq/day) diet. Nondiabetic control subjects (n=7) were evaluated under similar conditions. On low sodium intake, mean PRA levels were significantly reduced in the hypertensive diabetic group, but were not different between the control and normotensive diabetic groups. Hypertensive diabetic patients on high sodium intake also had greater reductions in PRA responses compared with the other study groups. In general, diabetic subjects on high sodium intake excreted less sodium and had more cumulative sodium retention than control subjects. Levels of inactive renin were not significantly different between the normotensive and hypertensive diabetic patients and were comparable with the levels in control subjects. Inactive renin levels changed in a similar direction and magnitude as PRA in response to sodium intake and posture in the three study groups. Infusion of angiotensin II led to comparable reductions in PRA in both diabetic groups and in the control group, suggesting an intact short feedback loop control. We conclude that Type II hypertensive diabetic patients with no or minimal complications have abnormalities of renin secretion that are best brought out under conditions of dietary sodium balance. The reduced PRA responses in these patients cannot be explained by defective activation of renin or by abnormalities of the angiotensin II short feedback loop of PRA control. Advanced age and abnormalities in renal sodium excretion in diabetic patients in combination with elevated blood pressure may account for the abnormal PRA responses in Type II diabetic hypertensive subjects. © 1989 American Heart Association, Inc.