Angiotensin II does not alter ACTH responses to hypoglycemia in conscious dogs.

Abstract

These experiments were designed to test for an interaction between angiotensin II (ANG II) and stress in the control of plasma adrenocorticotropin hormone (ACTH), corticosteroids, and aldosterone. The stimulus to ACTH used in this study was insulin-induced hypoglycemia, a stimulus that does not increase plasma ANG II concentrations. Five trained dogs with exteriorized carotid arteries were studied. Each dog was infused with ANG II intravenously (10 ng X kg-1 X min-1) or into the carotid artery (1 ng X kg-1 X min-1) or with saline (iv) for 80 min. Twenty minutes after the start of the infusion, insulin (0.10 U/kg iv) was injected. Intravenous infusion of ANG II increased mean arterial pressure (MAP) and plasma aldosterone concentrations but did not increase ACTH or corticosteroid responses to hypoglycemia. Intracarotid infusion of ANG II did not increase MAP and also failed to increase ACTH and corticosteroid responses to hypoglycemia. Since ANG II infusions did not increase basal corticosteroids, the failure of ANG II to stimulate ACTH is not a result of steroid negative feedback. Thus it appears that increased plasma ANG II concentrations do not increase ACTH responses to hypoglycemic stress.