Acute hypertension inhibits thirst stimulated by ANG II, hyperosmolality, or hypovolemia in rats

The present study sought to determine whether increases in arterial blood p ressure inhibited drinking behavior evoked by ANG II, hyperosmolality, or h ypovolemia in rats. Cumulative water intakes in 60- or 90-min tests and lat ency to the first lick were recorded as indexes of thirst. During intraveno us infusions of 100 ng.kg(-1).min(-1) ANG II, attenuation of the induced in creases in arterial pressure with the arteriolar vasodilator diazoxide resu lted in greater water intakes and shorter latencies to drink. Drinking beha vior stimulated by intravenous infusion of hypertonic saline was significan tly inhibited by increases in arterial pressure caused by intravenous infus ion of phenylephrine or endothelin-1, and this inhibition of drinking was p roportional to the induced increase in pressure. Upon termination of the ph enylephrine infusion, mean arterial pressure returned to basal values, and drinking was restored. Phenylephrine-induced increases in arterial pressure also inhibited drinking behavior in response to hypovolemia that could not be explained by differences in plasma renin activity, plasma protein conce ntration, or plasma osmolality. Thus increases in arterial pressure inhibit water drinking behavior in response to each of these three thirst stimuli in rats.