Insulin resistance, hypertension and cellular ion transport systems

Much epidemiological, physiological and biochemical evidence links insulin resistance and hyperinsulinaemia to the pathogenesis of hypertension in some metabolic diseases such as obesity and type 2 (non-insulin-depedent) diabetes mellitus. Insulin resistance per se, by altering the energy needs of the cell, by causing a shift from glucose to lipid metabolism, or by some other incompletely defined mechanisms, could be responsible for the development of hypertension. It is also possible that hyperinsulinaemia, by acting on the vascular tree, leads to an increase in blood pressure. Moreover, insulin has been shown to augment renal sodium reabsorption, to stimulate the sympathetic nervous system, to influence atrial natriuretic peptide release and the renin-angiotensin-aldosterone system and to activate a number of sodium pumps which are present in all cell membranes, including vascular smooth muscle cells. Insulin can also directly stimulate cell growth. All these mechanisms, in various combinations, with the concurrence of some genetic factors, could lead to the development of the association between hypertension and abnormalities in glucose metabolism.