Evidence Against a Central Pressor Mechanism for Adrenocortical Steroid Hypertension in Sheep

Abstract

The possibility that corticotropin (ACTH)-induced hypertension results from a direct central effect of the adrenocortical steroids released by ACTH was investigated in sheep. Using two approaches, steroid levels were increased in the brain while peripheral levels remained sub-pressor. The blood pressure response to intravenous infusion of a combination of 7 steroids (aldosterone, cortisol, deoxycorticosterone, corticosterone, 11-deoxycortisol, 17 alpha hydroxyprogesterone and 17 alpha 20 alpha dihydroxyprogesterone), which causes a similar pressor effect to ACTH, was compared with that caused by intracarotid infusion of the steroids at rates calculated to give concentrations in the brain equivalent to those achieved after intravenous infusion. We also examined the effects of infusing the combination of steroids directly into the central nervous system via the lateral cerebral ventricles. Intravenous infusion of the steroids increased mean arterial pressure (MAP) from a control average of 84.0 +/- 1.1mmHg to 98.2 +/- 2.2mmHg (p < 0.001) on day 5. There was no increase in MAP during intracarotid infusion, nor during intracerebroventricular infusion. These findings suggest that the adrenocortical steroids released by ACTH do not act directly on central steroid receptors to increase blood pressure.