High salt diet alters neural cardiovascular control. This influence has been attributed to central neural or efferent mechanisms. To test the hypothesis that a high salt diet might alter afferent baroreceptor function, Dahl salt-resistant (DR) and salt-sensitive rats (DS) were fed a high or a low salt diet. Blood pressure was measured intra-arterially in unanesthetized animals. Aortic baroreceptor function was then evaluated during urethane anesthesia by recording multifiber aortic depressor nerve activity during a phenylephrine-induced blood pressure ramp. Mean arterial pressure in the conscious state was elevated (155 ± 5 [SE] mm Hg) in DS fed a high salt diet but was normal in DS fed a low salt diet and in DR. Slopes of linear regressions relating aortic nerve discharge to mean arterial pressure were 71 % higher in DR fed a high salt diet than in DR fed a low salt diet (p< 0.025), indicating that high salt potentiated baroreceptor function in DR. In contrast, high salt diet produced no significant effects on baroreceptor function in DS. No salt-induced changes in dynamic or static aortic distensibility (assessed from pressure-volume curves of the in situ isolated arch) were detectable in either rat strain. Absence of salt-induced baroreceptor sensitization in DS was not due to the hypertensive state because the sensitization also failed to occur in separate groups of DS in which saltinduced hypertension had been prevented by chemical sympathectomy with 6-OH-dopamine. Thus, high dietary salt 1) potentiates afferent arterial baroreceptor function in DR, a phenomenon unrelated to aortic distensibility and probably resulting from sensitization of baroreceptors by high salt diet, and 2) fails to sensitize baroreceptors in DS, probably because of a primary abnormality in baroreceptor function in DS.