Activation by Angiotensin II of Ca 2+ -dependent K + and Cl − Currents in Zona Fasciculata Cells of Bovine Adrenal Gland

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.

T-Type Calcium Channel: A Privileged Gate for Calcium Entry and Control of Adrenal Steroidogenesis

“…Similar results have been obtained with adrenal fasciculata cells. Indeed, in bovine cells, AngII induces a biphasic response corresponding to a transient hyperpolarization followed by a sustained depolarization ( 141 ). The hyperpolarization phase appears to be due to the activation of calcium-dependent potassium currents, but also to chloride currents, the resting potential of fasciculata cells being less negative than that of glomerulosa cells.…”

Angiotensin II (AT1) Receptors and NADPH Oxidase Regulate Cl− Current Elicited by β1 Integrin Stretch in Rabbit Ventricular Myocytes

“…On the other hand, I CFTR,cardiac is strongly inhibited by AngII via AT1 receptors and inhibition of adenylate cyclase (Obayashi et al, 1997). AngII also activates a Ca 2ϩ -dependent Cl Ϫ current in mesangial (Marrero et al, 1996) and adrenal zona fasciculata cells (Chorvatova et al, 1998). In addition to effects on Cl Ϫ currents, AngII modulates a number of cation currents (for review see Chorvatova et al, 1996), and thus, integrin stretch-induced activation of AT1 receptors also may affect cardiac cation currents (Browe and Baumgarten, 2003b).…”

ANO4 (Anoctamin 4) Is a Novel Marker of Zona Glomerulosa That Regulates Stimulated Aldosterone Secretion

“…To establish the relationship between anoctamin expression and other channels already known to be active in the adrenal gland, we looked into published articles. Chloride currents recorded in the adrenal of human and nonhuman species have different characteristics from CaCCs: Chorvatova et al 34 described a Ras-dependent, transient chloride current activated by ACTH at low concentrations in bovine ZG cells through activation of Ras by β gamma subunits. 35 Spat et al examined Cl − currents with the patch-clamp technique in rat ZG cells.…”