ACTIVATION BY ANGIOTENSIN-II OF CA2-DEPENDENT K+ AND CL- CURRENTS IN ZONA-FASCICULATA CELLS OF BOVINE ADRENAL-GLAND()

Citation
A. Chorvatova et al., ACTIVATION BY ANGIOTENSIN-II OF CA2-DEPENDENT K+ AND CL- CURRENTS IN ZONA-FASCICULATA CELLS OF BOVINE ADRENAL-GLAND(), The Journal of membrane biology, 162(1), 1998, pp. 39-50
Citations number
35
Categorie Soggetti
Cell Biology",Biology
ISSN journal
00222631
Volume
162
Issue
1
Year of publication
1998
Pages
39 - 50
Database
ISI
SICI code
0022-2631(1998)162:1<39:ABAOCK>2.0.ZU;2-X
Abstract
The effects of angiotensin II (100 nM) on the electrical membrane prop erties of zona fasciculata cells isolated from calf adrenal gland were studied using the whole cell patch recording method. In current-clamp condition, angiotension II induced a biphasic membrane response which began by a transient hyperpolarization followed by a depolarization m ore positive than the control resting potential. These effects were ab olished by Losartan (10(-5) M), an antagonist of angiotensin receptors of type I. The angiotensin II-induced transient hyperpolarization was characterized in voltage-clamp condition from a holding potential of -10 mV. Using either the perforated or the standard recording method, a transient outward current accompanied by an increase of the membrane conductance was observed in response to the hormonal stimulation. Thi s outward current consisted of an initial fast peak followed by an osc illating or a slowly decaying plateau current. In Cl--free solution, t he outward current reversed at -78.5 mV, a value close to E-K. It was blocked by external TEA (20 mM) and by apamin (50 nM). In K+-free solu tion, the transient outward current, sensitive to Cl- channel blocker DPC (400 mu M), reversed at -52 mV, a more positive potential than E-C l. Its magnitude changed in the same direction as the driving force fo r Cl-. The hormone-induced transient outward current was never observe d when EGTA (5 mM) was added to the pipette solution. The plateau curr ent was suppressed in nominally Ca2+-free solution (47% of cells) and was reversibly blocked by Cd2+ (300 mu M) but not by nisoldipine (0.5- 1 mu M) which inhibited voltage-gated Ca2+ currents identified in this cell type. The present experiments show that the transient hyperpolar ization induced by angiotensin II is due to Ca2+-dependent K+ and Cl- currents. These two membrane currents are co-activated in response to an internal increase of [Ca2+](i) originating from intra- and extracel lular stores.