Insulin resistance and arterial hypertension

This review presents the role of insulin in the regulation of blood pressure, lipid and 
protein metabolism, body weight and transmembraneous transport of sodium, magnesium and calcium. Insulin resistance may be
 involved in the pathogenesis of essential hypertension. It results in a reduced sensitivity of 
insulin-mediated cellular glucose uptake which leads to a rise in plasma glucose and hence 
to a compensatory stimulation of insulin secretion in a attempt to normalize plasma glucose.
Thus, insulin resistance elicits a progressive 
rise in circulating insulin which induces a series
 of harmful changes, such as increased sodium
 and water reabsorption in the kidney tubules,
increased calcium and decreased magnesium
 content in cells, stimulation of sympathetic nervous system activity, and proliferation of vascular smooth muscle cells. These insulin-mediated alterations may promote hypertension. In
normal subjects insulin stimulates vascular smooth muscle calcium efflux and vascular relaxation. Some authors believe that insulin resistance is associated with decreased calcium
 efflux, which leads to sustained rise of calcium
 concentration in vascular smooth muscle cells. These data suggest that cellular insulin rather 
than hyperinsulinemia per se may lead to hypertension. Although it has been proposed that 
insulin resistance constitutes the major pathogenetic link between obesity, impaired glucose
 tolerance, type 2 diabetes, obesity, hyperlipemia and hypertension, it might well turn out that
 a common underlying abnormality (either acquired or inherited) promotes insulin resistance, on the one hand, and hypertension, overweight, hyperlipemia and glucose intolerance, on the other.