ABSTRACT
Individuals with elevated blood pressure are at increased risk for cardiovascular events and death. Almost 50% of essential hypertension is salt-sensitive, this characteristic increases and becomes more prevalent with age. Salt sensitivity has been linked to an increased risk for the development of left ventricular hypertrophy, proteinuria, and a blunted nocturnal decline in blood pressure ([quot ]non-dipping[quot ]). Salt sensitivity implies an alteration in the relation between arterial pressure and sodium excretion or [quot ]pressure natriuresis[quot ]. The development of salt-sensitive hypertension is proposed to occur in three phases. In the first phase, the kidney is structurally normal, and sodium is excreted normally. However, the kidney may be exposed to various stimuli that result in renal vasoconstriction. In the second phase, subtle renal injury develops, impairing sodium excretion and leading to an increase in blood pressure. In the third phase, the kidneys equilibrate at a higher blood pressure, allowing them to resume normal sodium handling. Other mechanisms, such as primary tubulointerstitial disease, genetic alterations in sodium regulation and excretion, or a congenital reduction in nephron number that limits sodium filtration are important in the development of salt-sensitive hypertension.