AJP - Endocrinology and Metabolism, Vol 255, Issue 1 E46-E53, Copyright © 1988 by American Physiological Society
Effects of CRF and ANG II on ACTH and vasopressin release in conscious dogs
C. K. Klingbeil, L. C. Keil, D. Chang and I. A. Reid
Department of Physiology, University of California, San Francisco 94143.
The aim of the present study was to examine the effects of
corticotropin-releasing factor (CRF) in conscious dogs and to determine
whether the stimulation of adrenocorticotropic hormone (ACTH) release by
angiotensin II (ANG II) results from potentiation of the action of CRF. In
addition, the possible role of CRF in the stimulation of vasopressin
released by ANG II was investigated. The following experiments were
performed: 1) intravenous saline infusion; 2) ANG II (10 ng.kg-1.min-1)
alone; 3) vasopressin (1 ng.kg-1.min-1) alone; 4) CRF (0.001, 0.01, or 0.1
microgram/kg iv) bolus; 5) vasopressin (1 ng.kg-1.min-1) and CRF (0.1
microgram/kg) together; 6) CRF (0.001, 0.01, or 0.1 microgram/kg) and ANG
II (10 ng.kg-1.min-1) together; 7) ANG II (10 ng.kg-1.min-1) followed 15
min later with CRF (0.001, 0.01, or 0.1 microgram/kg). Each dose of CRF was
tested on a different day. Infusion of ANG II alone stimulated the release
of ACTH, cortisol, and vasopressin. Administration of CRF produced
dose-dependent increases in plasma ACTH and cortisol concentrations, and
the highest dose of CRF increased plasma vasopressin concentration. CRF
given together with ANG II did not potentiate the stimulation of ACTH
release by CRF. Vasopressin at the dose tested did not stimulate ACTH
release but potentiated the ACTH response to CRF. ANG II stimulated
vasopressin release but did not potentiate the AVP response to CRF. These
results show that, in conscious dogs, ANG II and CRF each increase plasma
ACTH concentration and that the ACTH response to CRF is potentiated by
vasopressin but not by ANG II.(ABSTRACT TRUNCATED AT 250 WORDS)
