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Brattleboro Rats Have Deficient Adrenocorticotropin Responses to Activation of Central ₁-Adrenoceptors

Department of Endocrinology (S.A.-D., M.B.) and the William Harvey Research Institute (S.A.-D.), the Medical College of St. Bartholomew's Hospital, London; and the Department of Clinical Biochemistry, University of Manchester (A. W.) Manchester, United Kingdom

Address all correspondence and requests for reprints to: Dr. Saad Al-Damluji, Endocrinoloy and Reproduction Research Branch, Building 10, Room B1L400, National Institutes of Health, Bethesda, Maryland 20892.

Abstract

This experiment was designed to test further the hypothesis that vasopressin is the major mediator of the ACTH response to activation of central ₁-adrenoceptors in the rat. The a₁-adrenergic agonist methoxamine was given intracerebroventricularly to conscious vasopressin-deficient (homozygous Brattleboro) and normal rats bearing venous and intracerebroventricular cannulae. Methoxamine stimulated the secretion of ACTH in the normal, but not in the vasopressin-deficient, rats. The data confirm that vasopressin, rather than CRH-41 or oxytocin, is the major hypothalamic peptide that mediates the effects of central ₁-adrenoceptors on the pituitary corticotrophs. (Endocrinology 127: 2849–2853, 1990)

Received June 18, 1990.