Insulin and Hypertension: Introduction

Abstract

Arelationship between insulin and hypertension emerged in epidemiologic studies reported in the mid-1980s. The association of insulin with hypertension was most pronounced in obese hypertensive subjects but was noted in lean hypertensives as well. Although insulin is a direct vasodilator, it is also known to stimulate the sympathetic nervous system and promote renal sodium reabsorption, both potential mechanisms that might exert a prohypertensive effect. The observations that normotensive relatives of hypertensive patients demonstrate insulin resistance and the absence of insulin resistance in patients with secondary forms of hypertension both contributed to the possibility that insulin plays a role in the pathophysiology of essential hypertension. For these reasons, the relationship between insulin and blood pressure has blossomed into an area of considerable interest over the last decade. Multiple sessions devoted to this topic are common at national and international hypertension meetings. Debate at these sessions is, moreover, characteristically high spirited.

The actual role played by insulin in the pathogenesis of hypertension remains obscure. Definitive evidence of a causal role for insulin in initiating or maintaining essential hypertension in humans is lacking. Circumstantial evidence, on the other hand, abounds. In this Point/Counterpoint review, two authorities working in the field present their view of this relationship. Professor Hall and his colleagues have argued persuasively that experimental evidence, much of it from their own laboratories, does not support a role for insulin. Much of this experimental work, however, depends upon studies performed in the dog, and its relevance to human hypertension remains, therefore, problematic. Inferences drawn from patients with insulinoma (who lack hypertension) may be overstated since in insulinoma elevated insulin levels consist, at least in part, of proinsulin, and blood glucose levels tend to be low, rather than slightly elevated as they are in insulin-resistant subjects without insulinoma. If both insulin and glucose are involved in the prohypertensive process, this lower level of glucose might be an important distinguishing feature between patients with insulinoma and insulin resistant subjects with hypertension.