Vasodysfunction That Involves Renal Vasodysfunction, Not Abnormally Increased Renal Retention of Sodium, Accounts for the Initiation of Salt-Induced Hypertension

It has long been recognized that in some people substantially increasing dietary intake of salt (NaCl) increases blood pressure, whereas in others, “salt loading” has little or no effect on blood pressure.1 Blood pressure so affected by salt has been called salt sensitive and salt resistant, respectively. Although the blood pressure response to salt is a continuous variable and the trait of salt sensitivity, like that of hypertension, is arbitrarily defined,2 it has been estimated that 30% to 50% of hypertensive humans are salt sensitive and ≈25% of normotensive humans are salt sensitive.3,4 Salt sensitivity confers an increased risk for the occurrence of hypertension and cardiovascular disease.5–7 Furthermore, pathophysiological mechanisms mediating salt sensitivity may contribute to the risk for cardiovascular disease beyond their effects on blood pressure.5 Accordingly, the mechanisms of salt sensitivity continue to be studied intensively with the hope that better understanding of those mechanisms could lead to improved approaches to the prevention and treatment of salt-induced increases in blood pressure and cardiovascular disease.Response by Hall on p 893 Prevailing theory holds that an abnormally large increase in renal retention of salt8–16 is an early pathophysiological event in the causation of salt sensitivity and salt-induced hypertension. In accord with this theory, it is held that a substantial increase in dietary salt does not induce a pressor effect in salt-resistant subjects because they excrete a salt load more rapidly and retain less sodium than salt-sensitive individuals.12,17 In the present analysis, we challenge this conventional view of salt sensitivity/salt resistance and make the case for a “vasodysfunction” theory for the initiation of salt-induced hypertension: An abnormal vascular resistance response to increases in salt intake, in the absence of an abnormally large increase in renal …