NACL INJECTIONS IN BRAIN INDUCE NATRIURESIS AND BLOOD-PRESSURE RESPONSES SENSITIVE TO ANG-II AT(1) RECEPTORS

In the present study we tested the hypoth- esis that the natriuretic a nd presser effects of intracerebroventricularly (icy) injected hyperto nic saline involve a central angiotensinergic pathway. All experiments were performed in conscious Wistar rats. Bolus injections of hyperton ic saline (0.19, 0.23, 0.30, and 0.60 M icv; injection volume 5 mu l) induced a concentration-dependent increase of renal sodium excretion w ithout affecting urinary flow. The increase in renal sodium excretion after the two highest saline concentrations was accompanied by signifi cant increases in mean arterial blood pressure (MAP). Pretreatment wit h the angiotensin (ANG) AT(1) receptor antagonist, losartan (5 mu g ic v), reduced the natriuretic effect of 0.23 and 0.30 M saline but did n ot affect the natriuresis induced by 0.60 M saline. The increase in MA P after 0.30 and 0.60 M saline icy was markedly attenuated by intracer ebroventricular pretreatment with losartan. Our results demonstrate th e involvement of a central angiotensinergic mechanism in the natriuret ic and presser responses to hypertonic saline. In addition to the ANG II-mediated natriuresis, an additional natriuretic mechanism, independ ent of ANG II and associated with the saline-induced presser effect, s eems to be recruited with increasing concentrations of saline in the c erebrospinal fluid.