Acute hyperinsulinemia induces sodium retention and a blood pressure decline in diabetes mellitus.

Abstract

Hyperinsulinemia supposedly contributes to hypertension in diabetes mellitus. We sought to determine if the renal and cardiovascular effects of insulin are preserved in diabetes despite resistance to its glucose-lowering effect. We studied the effects of two doses of insulin (50 and 500 milliunits/kg.hr-1), using the euglycemic clamp technique, on fractional sodium excretion, blood pressure, and heart rate in two groups of non-insulin-dependent diabetics: eight patients with and eight patients without hypertension. Hypertensive diabetics had higher basal insulin levels than normotensive diabetics (21.8 +/- 2.9 and 14.4 +/- 1.6 milliunits/l, respectively [mean +/- SEM]; p = 0.03). The degree of insulin resistance, but not plasma insulin levels, correlated with the height of mean arterial blood pressure (r = 0.60 and 0.73 at the low and high insulin dose, respectively; p less than 0.05). In contrast, the change in mean arterial blood pressure correlated negatively with the change in endogenous insulin levels during the control experiment (r = -0.41, p less than 0.02). Exogenous insulin induced a similar reduction in fractional sodium excretion in normotensive and hypertensive diabetics (43 +/- 5.9% and 48 +/- 16.4% during the low insulin dose and 57 +/- 9.1% and 62 +/- 12.5% during the high insulin dose, respectively). A decline in blood pressure was noted that correlated with the whole body glucose uptake during the high insulin dose (r = 0.52, p less than 0.05). Since heart rate response and plasma norepinephrine level during the insulin clamp were comparable in both groups, an abnormality of the baroreceptor reflex is suggested. It appears that insulin resistance, but not insulin, is primarily related to hypertension. At the same time, insulin may still exert some effect on blood pressure by way of its renal or vasodilatory, or both, action.