Figure 3.

Reduced receptor responsiveness in tissues primarily involved in the metabolic effects of insulin causes decreased glucose uptake and, in turn, leads to a compensatory response of the pancreatic islets with hyperinsulinemia. Excess circulating insulin acting on renal receptors increases sodium reabsorption with extracellular volume expansion. In normal conditions, volume expansion down-regulates renal insulin receptors restoring a normal volume status. In some rat strains of hypertension associated with insulin resistance, the feedback mechanism that reduces insulin-mediated antinatriuresis is defective thereby leading to the persistence of volume expansion and increase in blood pressure.