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  • Title: Activation by angiotensin II of Ca(2+)-dependent K+ and Cl- currents in zona fasciculata cells of bovine adrenal gland.
    Author: Chorvatova A, Guyot A, Ojeda C, Rougier O, Bilbaut A.
    Journal: J Membr Biol; 1998 Mar 01; 162(1):39-50. PubMed ID: 9516236.
    Abstract:
    The effects of angiotensin II (100 nM) on the electrical membrane properties 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 more positive than the control resting potential. These effects were abolished by Losartan (10(-5) M), an antagonist of angiotensin receptors of type 1. 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. This outward current consisted of an initial fast peak followed by an oscillating or a slowly decaying plateau current. In Cl(-)-free solution, the outward current reversed at -78.5 mV, a value close to EK. It was blocked by external TEA (20 mM) and by apamin (50 nM). In K(+)-free solution, the transient outward current, sensitive to Cl- channel blocker DPC (400 microM), reversed at -52 mV, a more positive potential than ECl. Its magnitude changed in the same direction as the driving force for Cl-. The hormone-induced transient outward current was never observed when EGTA (5 mM) was added to the pipette solution. The plateau current was suppressed in nominally CA(2+)-free solution (47% of cells) and was reversibly blocked by Cd2+ (300 microM) but not by nisoldipine (0.5-1 microM) which inhibited voltage-gated Ca2+ currents identified in this cell type. The present experiments show that the transient hyperpolarization induced by angiotensin II is due to Ca(2+)-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 extracellular stores.
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