The vasodilator action of insulin. Implications for the insulin hypothesis of hypertension.

The last several years have witnessed tremendous interest in the hypothesis that insulin resistance and hyperinsulinemia contribute to the pathogenesis of hypertension. This hypothesis was stimulated by epidemiological studies that demonstrated an association between obesity, insulin resistance, and hypertension.Subsequent studies suggested that even lean individuals with essential hypertension have insulin resistance and hyperinsulinemia.' Because hyperinsulinemia persists during antihypertensive therapy and is not found in secondary renovascular hypertension, the hyperinsulinemia does not appear to be secondary to elevated arterial pressure. In addition to effects on glucose metabolism, insulin has sympathetic and renal actions.In obesity and hypertension, there is resistance to the actions of insulin on glucose uptake but no resistance to the renal and sympathetic actions of insulin. These "secondary" actions of insulin form the basis of the insulin hypothesis of hypertension.The insulin hypothesis proposes that the compensatory hyperinsulinemia that occurs with insulin resistance increases sodium reabsorption and sympathetic activity, which combine to cause elevated arterial pressure.An implicit and important assumption of this hypothesis is that, because insulin increases sympathetic noradrenergic activity, it increases vascular resistance and arterial pressure. This editorial will discuss the vasodilator (depressor) action of insulin and the role that this action plays in offsetting the sympathetic and antinatriuretic (pressor) actions of insulin in regulating arterial pressure. The vasodilator actions of insulin have important implications for the insulin hypothesis of hypertension.