AJP - Regulatory, Integrative and Comparative Physiology, Vol 248, Issue 3 363-R370, Copyright © 1985 by American Physiological Society
Central role for angiotensin in control of adrenal catecholamine secretion
E. J. Corwin, J. F. Seaton, M. Hamaji and T. S. Harrison
Angiotensin II (ANG II) is required for unimpaired adrenal reflex secretion
of catecholamines after hemorrhage in the dog. To test if ANG II acts
centrally, experiments were performed under general anesthesia on
bilaterally or sham-nephrectomized dogs hemorrhaged at 25 ml/kg.
Ventriculocisternal perfusion of ANG II or its antagonist saralasin was
accomplished via needles inserted in the left lateral cerebral ventricle
and cisterna magna. Mean arterial pressure and adrenal secretion of
catecholamines were measured before and after hemorrhage. Nephrectomized
dogs receiving only artificial cerebrospinal fluid (CSF) by
ventriculocisternal perfusion had a very small adrenal response to
hemorrhage compared with animals receiving ANG II intraventricularly (IVT)
(at 10 and 100 pg . kg-1 . min-1). This effect of ANG II IVT also depended
on the rate of IVT infusion. Peripheral infusion of ANG II (10 pg . kg-1 .
min-1) had no effect on adrenal catecholamine secretion. Animals with
intact kidneys given saralasin IVT (0.06 ng/min) responded similarly to
nephrectomized dogs receiving only CSF IVT. Intravenous saralasin did not
blunt the response to hemorrhage. Thus ANG II appears to support
catecholamine secretion via a central mechanism. This mechanism is
physiologically significant because either nephrectomy or functional
elimination of ANG II by saralasin greatly attenuates the adrenal medullary
response to hemorrhage in vivo.
