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.