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 Conlin, P. R.
Right arrow Articles by Canessa, M. L.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Conlin, P. R.
Right arrow Articles by Canessa, M. L.

Endocrinology, Vol 129, 1861-1868, Copyright © 1991 by Endocrine Society

ARTICLES

Angiotensin II-induced activation of Na(+)-H+ exchange in adrenal glomerulosa cells is mediated by protein kinase C

PR Conlin, GH Williams and ML Canessa
Department of Medicine, Brigham and Women's Hospital, Boston, Massachusetts 02115.

Modulation of Na(+)-H+ exchange (Na/H EXCH) by hormones and growth factors may be important in cell growth. We have previously shown that Na/H EXCH in adrenal glomerulosa cells is activated by angiotensin II (ANG II), a potent stimulator of aldosterone secretion. In the present paper, we have investigated the role of protein kinase C (PKC) in the activation of Na/H EXCH by ANG II. To accomplish this, we monitored cytosolic pH (pHi) in cells loaded with 2,7-biscarboxyethyl-5 (6)- carboxyflourescein and measured initial rates off 22Na uptake into glomerulosa cells in the presence or absence of dimethylamiloride. Both phorbol 12-myristate 13-acetate (PMA) and ANG II increased the activity of Na/H EXCH similarly when studied under basal conditions (pH 7.1). This was accompanied by alkalinization of pH and an increase in dimethylamiloride-sensitive Na+ influx. Study of kinetics of the antiporter activation showed that both ANG II and PMA led to an increase in the maximal rate (Vmax) and a decrease in the Michaelis- Menten constant (Km) for external Na+. The pHi dependence of Na+ influx was half-minimal (pK) at pHi 7.09 and remained unchanged in the presence of ANG II (pK 7.03) and PMA (pK 7.14). Depleting the cells of PKC by exposing them to PMA (1 microM) for 3 h caused a marked reduction in control and ANG II-stimulated Na+ influx and control pK (7.09 to 6.85, P less than 0.05). However, with PKC depletion, the kinetics of Na/H EXCH (Vmax, Km for external Na+, and pK) were unaffected by ANG II. Thus, Na/H EXCH in adrenal glomerulosa cells functions under basal conditions, and its relatively alkaline pK (7.09) is dependent upon PKC activity. In addition, the ANG II-induced activation of Na/H EXCH is modulated by PKC. These effects suggest an important role for PKC in pHi regulation of adrenal glomerulosa cells, particularly during ANG II stimulation of aldosterone secretion.


This article has been cited by other articles:


Home page
 Physiol. Rev.Home page
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]

Home page
 Pharmacol. Rev.Home page
G. G. Nussdorfer, G. P. Rossi, L. K. Malendowicz, and G. Mazzocchi
Autocrine-Paracrine Endothelin System in the Physiology and Pathology of Steroid-Secreting Tissues
Pharmacol. Rev., September 1, 1999; 51(3): 403 - 438.
[Abstract] [Full Text] [PDF]


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 © 1991 by The Endocrine Society