[Salt-dependent arterial hypertension]

Almost 50% of essential hypertension is salt-sensitive, this characteristic increases and becomes more prevalent with age and is associated with a greater risk of cardiovascular a renal complications. The mechanism responsible for it has not been well established yet, although the participation of several vasoactive factors has been involved. Salt sensitivity implies an alteration in the relation between arterial pressure and sodium excretion or "pressure natriuresis", which is shifted to the right, that is, a higher blood pressure is required to maintain normal sodium excretion. Experimental studies suggest that this alteration is mediated by an increase in the resistance of preglomerular vessels due to hypertrophy of the vascular wall, decreased glomerular permeability, and enhanced tubular sodium reabsorption, as well as tubulointerstitial alterations that result in local release of vasoactive factors, cytokines, and growth factors, which, in turn, enhance glomerular hemodynamic alterations and impair sodium excretion.