SALT INTAKE AND PLASMA ATRIAL-NATRIURETIC-PEPTIDE AND NITRIC-OXIDE INHYPERTENSION

In response to a high salt intake, salt-sensitive hypertensive individ uals retain more sodium and manifest a rise in blood pressure greater than that in salt-resistant individuals. In this study, we tested whet her salt sensitivity might be related at least in part to reduced secr etion of atrial natriuretic peptide (ANP) or to abnormal nitric oxide production. We measured plasma ANP and NO2+NO3 in 7 normotensive indiv iduals and 13 salt-sensitive and 14 salt-resistant blacks with essenti al hypertension under conditions of low (10 mEq/d) and high (250 mEq/d ) salt intake. To evaluate possible racial differences in ANP secretio n, we also measured plasma ANP in 6 salt-sensitive and 8 salt-resistan t hypertensive whites during low and high salt intakes. Under low salt conditions, plasma ANP levels were not different in normotensive cont rol subjects and salt-sensitive and salt-resistant hypertensive blacks . During high salt intake, plasma ANP levels did not change in control subjects and salt-resistant patients but decreased in salt-sensitive patients. ANP levels after high salt diet were lower (P<.01) in salt-s ensitive than salt-resistant blacks. In hypertensive whites, high salt intake caused no significant change in plasma ANP. Under low salt con ditions, plasma NO2+NO3 levels were higher (P<.05) in salt-sensitive ( 189+/-7.9 mu mol/L) and salt-resistant (195+/-13.5 mu mol/L) black pat ients than in control subjects (108+9.7 mu mol/L). During high salt in take, plasma NO2+NO3 decreased significantly (P<.01) in both salt-sens itive (150+/-7.0 mu mol/L) and salt-resistant (142+/-9.0 mu mol/L) pat ients. These studies show that under conditions of high salt intake, s alt-sensitive hypertensive blacks manifest a paradoxical decrease in A NP secretion. This abnormality may play a role in tile reduced ability of these individuals to excrete a sodium load and in the sodium-induc ed rise in blood pressure. This study does not support the hypothesis that salt sensitivity depends on a deficit of nitric oxide production, but it suggests that high salt intake may alter the endothelium-depen dent adaptation of peripheral resistance vessels.