Previous studies have shown that essential hypertension is frequently associated with insulin resistance and hyperinsulinism. Because insulin may exert a direct positive inotropic as well as chronotropic effect and controlled the initiation of peptide chains in the heart, we tested the hypothesis that insulin may be a determinant of myocardial hypertrophy and contractility. The relation between glucose metabolism (assessed by the oral glucose tolerance test) and left ventricular (LV) mass and function (assessed by echocardiography) was explored in 47 never-treated lean essential hypertensive patients (EH) of short duration and 19 normotensive subjects (NT). A greater number of EH versus NT (23 vs 5%) had an abnormal glucose tolerance. The fasting insulin-to-glucose ratio was significantly higher in EH as compared to NT. Fasting as well as integrated serum insulin to glucose values ratio were positively correlated with heart rate (r = 0.35, p < 0.05, r = 0.38, p < 0.05) and the LV end-systolic stress to volume ratio (r = 0.48, p < 0.001, r = 0.54, p < 0.001) but not with LV mass (r = 0.02, r = 0.02) in EH. When EH were divided into those with normal (n = 36) and supernormal (n = 11) LV contractility based on the relationship between LV fractional shortening and LV end-systolic stress, integrated insulin level and fasting insulin to glucose ratio were markedly higher in patients with supernormal LV contractility, whereas arterial pressure, heart rate, urinary sodium excretion, and plasma renin activity were similar in the two groups. We concluded that hyperinsulinemia and LV hypercontractility are associated in patients with hypertension of short duration. If chronic hyperinsulinemia is to be causally related to hypertension, one would have to postulate that the effects (inotropism and chronotropism) of insulin on the heart can be dissociated from the resistance to the glucose-lowering action of insulin.