help button home button Endocrine Society Endocrinology
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS

This Article
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow Request Copyright Permission
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Horiuchi, T.
Right arrow Articles by De Lean, A.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Horiuchi, T.
Right arrow Articles by De Lean, A.

Endocrinology, Vol 124, 1925-1931, Copyright © 1989 by Endocrine Society


ARTICLES

Regulation of aldosterone biosynthesis by Na+/H+ antiport: relationships between intracellular pH and angiotensin II

T Horiuchi, TT Nguyen, EJ Cragoe Jr and A De Lean
Laboratory of Molecular Pharmacology, Clinical Research Institute of Montreal, Quebec, Canada.

Recent studies on the regulation of aldosterone biosynthesis have revealed that inhibitors of sodium influx, e.g. amiloride, can inhibit adrenal steroidogenesis with a pharmacological profile suggestive of a Na+/H+ antiport system. We have examined the existence of a Na+/H+ antiport system and its regulation of Na influx and intracellular pH (pHi) in bovine adrenal zona glomerulosa cells. NH4Cl-induced 22Na uptake by zona glomerulosa cells was dose dependently inhibited by ethylisopropylamiloride (EIPA), amiloride, and benzamil with ED50 values of 0.02, 4.30, and 199 microM, respectively. Angiotensin II (AII; 100 nM) caused an initial transient acidification, followed by prolonged alkalinization. The hormone equipotently increased pHi and stimulated aldosterone secretion, with ED50 values of 1.2 and 1.4 nM, respectively. AII-induced alkalinization was suppressed by EIPA, amiloride, and benzamil, with ED50 values of 0.6, 79, and 440 microM, respectively. This increase in pHi induced by AII was dependent upon the extracellular sodium concentration (ED50 values = 2.8 mM) and was blunted in sodium-free medium. AII-stimulated aldosterone synthesis was also inhibited by EIPA, amiloride, and benzamil, with ED50 values of 0.07, 34, and 330 microM, respectively. The time course of activation by angiotensin II on aldosterone secretion was also dependent upon extracellular sodium concentration during a 2-h period. These results document that intracellular pH is regulated through the Na+/H+ exchange system and suggest that the pH change induced by AII might be associated with its regulation of steroidogenesis in bovine adrenal zona glomerulosa cells.


This article has been cited by other articles:


Home page
EndocrinologyHome page
H. Raff, B. M. Jankowski, E. D. Bruder, W. C. Engeland, and M. K. Oaks
The Effect of Hypoxia from Birth on the Regulation of Aldosterone in the 7-Day-Old Rat: Plasma Hormones, Steroidogenesis in Vitro, and Steroidogenic Enzyme Messenger Ribonucleic Acid
Endocrinology, July 1, 1999; 140(7): 3147 - 3153.
[Abstract] [Full Text]




HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Endocrinology Endocrine Reviews J. Clin. End. & Metab.
Molecular Endocrinology Recent Prog. Horm. Res. All Endocrine Journals
Copyright © 1989 by The Endocrine Society