Exogenous corticosterone acetate attenuates the hypotension induced by ganglion blockade in conscious Long Evans and Brattleboro rats.

The effects of acute administration of corticosterone acetate (7.5 mg/kg bolus; 5 mg.kg-1h-1 infusion) on plasma corticosterone levels and blood pressure (BP) responses to hypotension induced by ganglion blockade (with pentolinium) were studied in conscious Long Evans and Brattleboro (vasopressin-deficient) rats. Steroid infusion raised plasma corticosterone levels similarly in both strains of rat, but there was no effect on resting BP. However, the fall in BP after pentolinium administration was less in the steroid-treated groups of both strains than in their vehicle-injected counterparts. During infusion of pentolinium the ensuing recovery in BP was abolished by captopril administration. Steroid treatment did not affect this recovery but did attenuate the hypotensive effects of captopril. In Long Evans rats, only, there was a further vasopressin-mediated, recovery in BP during the infusion of pentolinium and captopril. This recovery was not accentuated by the presence of the steroid. In a further experiment, infusion of corticosterone acetate after the onset of hypotension (induced by pentolinium, captopril and d(CH2)5DAVP in Long Evans rats or by pentolinium and captopril in Brattleboro rats) caused a progressive increase in BP in both strains. These findings demonstrate a pressor action of corticosterone acetate which is apparent after hypotension induced by ganglionic blockade and which does not necessarily involve any interaction with the renin-angiotensin system or vasopressin.