Steroidogenesis and ionic permeability in adrenal glomerulosa cells.

Abstract

Over the past several years it has become possible to study some of the electrical properties of excitable and endocrine cells by measuring fluxes of radioactive tracer ions; 86Rb fluxes has been widely used to study potassium permeability. We have validated this approach in adrenal glomerulosa cells, in which we demonstrated the presence of a Ca-dependent K channel that is activated by angiotensin II, ATP, the ionophore A23187 and external K. Here, we present evidence that the steroidogenic response of the bovine adrenal glomerulosa cells is related, in the case of angiotensin II, to the inhibitory effect to the hormone on the coefficient rate of 86Rb efflux that occurs after the initial transient increase. This inhibition of the potassium permeability is probable responsible of the depolarization of the cells. Apamin, that blocks the initial transient raise on 86Rb efflux mediated by angiotensin II, has a minor stimulatory action on the hormone induce steroidogenesis; whereas the opposite is true for the steroidogenic action of potassium ions in the presence of apamin. The second groups of experiments examined the effect of angiotensin II on 86Rb fluxes when the Ca in the medium was increased from 0.6 to 1.25 mM in the case of bovine glomerulosa cells or angiotensin was assayed in rat glomerulosa tissue perifused with 0.6 mM Ca; in both conditions only the inhibitory effect in 86Rb efflux was observed. When the effect of external ATP on steroidogenesis was examined a significant increase on aldosterone secretion occurred probable by a similar mechanism. These results are indicative that Ca-mediated K efflux in adrenal glomerulosa cells may provide a modulatory mechanism for agonist action.