Adrenergic Mechanisms Involved in the Control of Pituitary-Adrenal Activity in the Rat: A β-Adrenergic Stimulatory Mechanism

Abstract

Epinephrine or isoproterenol was infused into a lateral tail vein of female Wistar rats under Nembutal anesthesia. After 20 min of infusion, trunk blood was collected for the determination of plasma corticosterone (B) and ACTH immunoreactivity (ACTH_i). Infusion of l-epinephrine resulted in a dose-related increase in plasma ACTH_i and B. Maximal levels were similar to those observed during ether stress. The pituitaryadrenal system appeared more sensitive than the cardiovascular system to epinephrine, since the ED₅₀ values of epinephrine for its effects on ACTH_i and heart rate were 165 and 840 ng/kg · min, respectively. The effect of epinephrine on pituitary-adrenal activity could be mimicked by the β-adrenergic agonist l-isoproterenol and could be blocked by the β-adrenergic antagonist l-propranolol, whereas d-propranolol was ineffective. The response of the pituitary-adrenal system to epinephrine was not caused by effects on peripheral parameters such as the distribution or clearance of ACTH or B but was mediated by an increase in ACTH release. The pituitary-adrenal response to epinephrine and isoproterenol was not related to changes in heart rate, blood pressure, or vasopressin secretion. Infusion of epinephrine at a dose that induced a maximal increase in plasma ACTH_i and B (1000 ng/kg · min) resulted in a circulating epinephrine concentration of 11 pmol/ml, which is within the physiological range. From these data we conclude that 1) circulating epinephrine can stimulate pituitary-adrenocortical activity, 2) this action is mediated by a β-adrenergic receptor mechanism, and 3) such a mechanism may be involved in the response of the pituitary-adrenal axis during certain forms of stress.