Diabetes may be associated with systolic hypertension secondary to atherosclerosis, renal hypertension secondary to diabetic nephropathy, and essential hypertension. The latter is by far the most prevalent, and a wealth of epidemiologic data suggests that such an association is independent of age and obesity. Considerable evidence indicates that the link between diabetes and essential hypertension is hyperinsulinemia. Thus, when hypertensive subjects, whether obese or of normal body weight, are compared to age- and weight-matched normotensive controls, a heightened plasma insulin response to a glucose challenge is found consistently. A state of cellular resistance to insulin action subtends the observed hyperinsulinism. With the use of the glucose clamp technique coupled with tracer glucose infusion and indirect calorimetry, it can be shown that the insulin resistance of essential hypertension is located in peripheral tissues (muscle), is limited to nonoxidative pathways of glucose disposal, and is directly correlated with the severity of hypertension. The reasons for the association of insulin resistance and essential hypertension can be sought in at least four general types of mechanisms--sodium retention, sympathetic nervous system overactivity, disturbed membrane ion transport, and altered muscle fiber composition. Physiologic maneuvers such as caloric restriction in the overweight individual and regular physical exercise can improve tissue sensitivity to insulin; good preliminary evidence shows that these measures can also lower blood pressure in both normotensive and hypertensive individuals. A strong case can therefore be made for the use of physiologic intervention in the treatment of essential hypertension.