Sympathetic hyperactivity elevates blood pressure during acute cerebroventricular infusions of hypertonic salt in rats.

Hypertonic solutions of 0.3 M sodium chloride (NaCl) infused into the third ventricle (ICV) for 20 min in urethane-anesthetized rats consistently elevated mean aortic pressure by approximately 10 mm Hg. Heart rate and sympathetic nerve activity diminished slightly during the first few minutes but then accelerated to attain higher than preinfusion levels. By contrast, ICV infusions of either artificial cerebrospinal fluid alone or 0.6 M sucrose were ineffective, those of 0.6 M urea were slightly depressor, while those of 0.3 M ammonium chloride elevated blood pressure without affecting sympathetic nerve activity. In rats pretreated with a vasopressin antagonist, the early pressor effects of hypertonic NaCl were inhibited, while sympathetic nerve firing, instead of being initially inhibited, increased from the onset. Consequently, the blood pressure elevation occurring during the first 5 min of ICV infusion was considered partly due to vasoconstriction caused by increased secretion of endogenous vasopressin, and subsequent maintenance of the blood pressure elevation after the first 10 min was attributed to sympathetic overactivity. Because pressor and sympathetic nerve responses were substantially enhanced following bilateral vagotomy or sinoaortic denervation, it was considered likely that responsiveness to hypertonic NaCl in intact rats in inhibited by both cardiopulmonary and sinoaortic baroreceptor afferents. Augmentation of pressor responsiveness following interruption of baroreceptor afferent pathways suggests that increases in sympathetic activity and blood pressure produced by hypertonic NaCl could contribute to salt-induced hypertension, particularly when baroreceptor buffering becomes deficient.