Mechanism of action of beta-endorphin and naloxone in hypophysectomized rats with hemorrhagic shock--the role of CNS.

The studies were performed on hypophysectomized rats with hemorrhagic shock treated intracerebroventricularly (i. c. v.) or intravenously (i. v.) by naloxone. The purpose of the investigation was to elucidate whether pituitary beta-endorphin (beta E) contribute to the hypotension and cardiodepressor changes during hypovolemic shock, the role of CNS opioid receptors for these effects, and the mechanism of action of naloxone. The results showed: The cardiorespiratory and hormonal changes in hypophysectomized rats represent an excellent model for the evaluation of the effects of some hormones, blockers or inhibitors, after either i. c. v. or i. v. administration. Neither i. c. v. nor i. v. administration of naloxone on hypophysectomized rats prevented the cardiodepressor changes during hemorrhagic shock. The beneficial effect of naloxone in hemorrhagic shock, manifested only on animals with intact pituitary glands, suggested that its therapeutic effect is mediated by CNS opioid receptors, and pituitary beta E may potentiate the hypotension during hypovolemic shock through an action on opiate receptors in the CNS. In hypophysectomized rats naloxone did not stimulate aldosterone secretion as it did in non-hypophysectomized rats with hemorrhagic shock, which indicated that this effect is secondary, accomplished by stimulation of the secretion of both ACTH and beta E.