Genetic and nongenetic determinants of salt sensitivity and blood pressure

Abstract

Salt sensitivity is characterized by an alteration of kidney function that necessitates higher arterial pressure to excrete a given amount of sodium and is expressed as a reduction in the slope of the pressure-natriuresis relation. Excess renal exposure to catecholamines, angiotensin II, aldosterone, and other mineralocorticoids all reduce the sensitivity of the pressure-natriuretic relation and lead to salt sensitivity. Inhibition of these pathways has opposite effects, as do excess circulating atrial natriuretic peptide and overactivity of various intrarenal paracrine systems, including vasodilator and natriuretic products of arachidonic acid metabolism, such as prostaglandin E2 and kinins. Salt sensitivity can also be inherited and ongoing studies are attempting to identify the genes that contribute to this trait. Abnormalities of renal function of Dahl salt-sensitive rats appear to precede the hypertension resulting from high salt intake. Although polymorphic differences have been identified between the Dahl salt-sensitive rat and normotensive rats, the specific genes contributing to the salt sensitivity have not yet been determined.