SALT SENSITIVITY - CONCEPT AND PATHOGENESIS

Almost two decades ago, the existence of a subset of essential hyperte nsive patients, who were sensitive (according to the increase in blood pressure levels) to the intake of a diet with a high salt content, wa s described. These patients are characterized by an increase in blood pressure and in body weight when switched from a low to a high sodium intake. The increase in body weight is due to the incapacity of the ki dneys to excrete the whole intake of sodium until renal perfusion pres sure (mean blood pressure) attains a level that is able to restore pre ssure-natriuresis relationship to values that enable the kidney to exc rete the salt ingested or administered intravenously. Salt sensitivity does not seem to depend on the existence of an intrinsic renal defect to handle sodium, but on the existence of subtle abnormalities in the regulation of the sympathetic nervous system, the renin-angiotensin s ystem or endothelial function. It is also relevant that organ damage s econdary to arterial hypertension, has been shown in animal models and in hypertensive humans sensitive to a high salt intake to be signific antly higher when compared with that of salt-resistant animals or huma ns. Interestingly, in humans, salt sensitivity has been shown to corre late with microalbuminuria, an important predictor of cardiovascular m orbidity and mortality, which correlates with most of the cardiovascul ar risk factors commonly associated with arterial hypertension. One of these factors is insulin resistance, that usually accompanies high bl ood pressure in overweight and obese hypertensives. Insulin resistance and hyperinsulinism are present in a significant percentage of hypert ensive patients developing cardiovascular symptoms or death. For these reasons, therapy of arterial hypertension must be directed, not only to facilitate the lowering of BP level, but also, to halt the mechanis ms underlying the increase in BP, when salt intake is increased. Furth ermore, therapy must preferably improve the diminished insulin sensiti vity present in salt-sensitive subjects that contribute independently to increased cardiovascular risk. (C) 1998 Elsevier Science Ireland Lt d. All rights reserved.