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.