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
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.