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1 Section of Anatomy, Department of Human Anatomy and Physiology, University of Padua, I-35121 Padua, Italy; and 2 Department of Histology and Embryology, School of Medicine, PL-60781 Poznan, Poland
This study
examined the effect of the pharmacological manipulation of adrenal
renin-angiotensin system (RAS) on aldosterone secretion from in situ
perfused adrenals of rats kept on a normal diet and sodium restricted
for 14 days. Neither the angiotensin-converting enzyme inhibitor
captopril nor the nonselective angiotensin II receptor antagonist
saralasin and the AT1 receptor-selective antagonist losartan affected basal aldosterone output in normally fed rats. In
contrast, they concentration dependently decreased aldosterone secretion in sodium-restricted animals, with maximal effective concentration ranging from 10
7 to
10
6 M. Captopril
(10
6 M), saralasin
(10
6 M), and losartan
(10
7 M) counteracted aldosterone
response to 10 mM K+ in sodium-restricted rats but not in
normally fed animals. Collectively, these findings provide evidence
that adrenal RAS plays a role in the regulation of aldosterone
secretion, but only under conditions of prolonged stimulation of zona
glomerulosa probably leading to overexpression of adrenal RAS.
in situ adrenal perfusion
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