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 La 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 abnormabties 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. (Hypertension 1989; 13:200-205)

Nonmodulation as the Mechanism for Salt Sensitivity of Blood Pressure in Individuals with Hypertension and Type 2 Diabetes Mellitus

“…Previous studies suggest that a positive relationship between T2DM and salt sensitivity exists, and this relationship is driven by low PRA levels and an increased frequency of LR status (5)(6)(7)30). Our carefully controlled human study refutes these observations.…”

The renin-angiotensin system in blacks: Active, passive, or what?

“…It is by indirect approaches that we have studied renal hemodynamics in several groups, including blacks. We studied renal perfusion and function in 32 healthy blacks and 82 age-matched healthy whites on a high-salt diet [26]. Although the glomerular filtration rate was similar, RPF was significantly less in age-matched blacks (568 ± 18) than whites (620 ± 13 mL/min/1.73 m 2 ; P = 0.0063) (Fig.…”

“…As PRA was identical in these healthy whites and blacks, the findings suggest that it is the intrarenal-renin system that is activated in blacks. Intrarenal activation of angiotensin II would operate via the short feedback loop to suppress systemic levels of renin, a paradoxic response [26]. If the kidneys of blacks were activated with angiotensin II, this would cause more vasoconstriction with resultant increased susceptibility to injury, especially when diseases like hypertension are superimposed.…”

Salt intake, hypertension and diabetes mellitus

“…25 Another controversial issue is whether or not patients with type 2 diabetes have a poorly suppressible renin release in response to a high salt diet. 26 When comparing renin-angiotensin-aldosterone system (RAAS) in hypertensive patients suffering from a non-late stage type 2 diabetes and essential hypertensives without diabetes, a higher incidence of low renin state was found in patients with essential hypertension. 21 Those authors observed an identical incidence of non-modulators in patients with essential hypertension or type 2 diabetes after exclusion of the low renin patients.…”