The crosstalk between insulin and the sympathetic nervous system: possible implications in the pathogenesis of essential hypertension.

Patients with non-insulin dependent diabetes mellitus and obesity show an elevated risk for development of arterial hypertension, while many non-obese, non-diabetic patients with essential hypertension display resistance to insulin-induced glucose disposal, accompanied by hyperinsulinaemia. This close association has lead some investigators to postulate that insulin resistance could be implicated in the pathogenesis of essential hypertension. Among the various factors considered as potential links between insulin resistance and high blood pressure, the sympathetic nervous system can be considered a prime candidate. In particular, our recent data in hypertensive patients have documented that the muscle sympathetic response evoked by insulin is about threefold greater than that observed in normal subjects. Such finding is well in agreement with previous observations in hypertensives obtained with experimental maneuvers and extends them by showing an abnormal sympathetic response to a physiological stimulus like insulin, so important in every day life. Recent data both from our and other laboratories have clearly established that an acute activation of sympathetic nervous system is able to antagonize insulin-mediated glucose uptake in the skeletal muscle, making very real the possibility that a primary defect in insulin sensitivity in hypertension may be further aggravated by the greater sympathetic response evoked by episodic stimuli, such as postprandial hyperinsulinaemia. However, while insulin evokes an increase in sympathetic nervous activity, at same time it is able to blunt the vasoconstrictive effects caused by the reflex sympathetic activation. Such vascular modulating effect of insulin is lost in essential hypertension, indicating that the resistance to insulin effect in this disease is not only present in skeletal muscle metabolism but it is also evident at the vascular level.