HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Vinson, G. P. Articles by Hinson, J. P. Search for Related Content PubMed PubMed Citation Articles by Vinson, G. P. Articles by Hinson, J. P.

Recent data have implicated the phosphatidylinositol/calcium second-messenger system in the control of aldosterone secretion by the adrenal zona glomerulosa. However, in the rat adrenal there are few reports of a direct effect of protein kinase C activation on steroid secretion, while the effects of calcium mobilization may be variable. Since the rat adrenal zona glomerulosa is sensitive to the mode of tissue preparation, these mechanisms were reinvestigated in intact (non-dispersed) capsular tissue and collagenase-dispersed zona glomerulosa cells.

Steroidogenesis in the intact zona glomerulosa was markedly affected by agonists of the calcium messenger system. Most notably, aldosterone and 18-hydroxycorticosterone (18-OH-B) secretion were stimulated by A23187 [GenBank] (100 nmol to 10 µmol/l) and BAY K 8644 (500 nmol/l). Phorbol 12-myristate 13-acetate (TPA; 1 pmol to 1 µmol/l) stimulated aldosterone secretion at all doses and caused a dose-dependent increase in 18-OH-B and 18-hydroxydeoxycorticosterone (18-OH-DOC) secretion. Corticosterone secretion was slightly increased in the presence of A23187 [GenBank] but not by TPA or BAY K 8644. Production of 18-OH-DOC was unaffected by A23187 [GenBank] and BAY K 8644. The calcium channel antagonist verapamil (10 µmol/l) inhibited ACTH-stimulated aldosterone secretion by the intact zona glomerulosa but had no effect on corticosterone secretion.

Verapamil (10 µmol/l) also inhibited the increase in aldosterone secretion by collagenase-dispersed zona glomerulosa cells stimulated by ACTH (100 fmol to 100 nmol/l), angiotensin II (100 pmol to 10 nmol/l) and potassium (5·9 and 8·4 mmol/l); stimulated corticosterone secretion was unaffected. Aldosterone secretion by dispersed zona glomerulosa cells was unaffected by the calcium ionophore A23187 [GenBank] (10 nmol to 100 µmol/l) or by TPA (1 nmol to 10 µmol/l). Corticosterone secretion was also unaffected by A23187 [GenBank] over the same dose range, but was increased slightly by high doses of TPA (10 and 1 µmol/l), while the calcium channel agonist BAY K 8644 had no effect on either steroid.

The results show that calcium mobilization and protein kinase C activation can stimulate steroid secretion in the rat adrenal zona glomerulosa and that large and reproducible effects are seen when intact tissue is used. In general only 18-OH-B and aldosterone secretion were affected; effects on corticosterone and 18-OH-DOC were much less marked. Together with the effects of calcium blockers, the data strongly support the view that protein kinase C activation and calcium mobilization are primarily involved in the control of the 'late pathway' of aldosterone biosynthesis.

This article has been cited by other articles:

				A. SPAT and L. HUNYADY Control of Aldosterone Secretion: A Model for Convergence in Cellular Signaling Pathways Physiol Rev, April 1, 2004; 84(2): 489 - 539. [Abstract] [Full Text] [PDF]

				G. A. Hines and R. Azziz Impact of Architectural Disruption on Adrenocortical Steroidogenesis In Vitro J. Clin. Endocrinol. Metab., March 1, 1999; 84(3): 1017 - 1021. [Abstract] [Full Text]