The role of calcium ions in rat Leydig cell steroidogenesis induced by atrial natriuretic peptide.

Abstract

The aim of this study was to clarify whether calcium ions play a role in the mechanisms by which rat atriopeptin II exerts its stimulatory effects on rat Leydig cell steroidogenesis. The absence of calcium in the medium and the calcium channel-blocker drug, verapamil, both significantly inhibited testosterone production in rat atriopeptin II-treated rat Leydig cells. Similar effects were observed on human chorionic gonadotropin-stimulated Leydig cells. Furthermore, 8-Bromoguanosine 3':5' cyclic monophosphate, the putative second messenger of atrial natriuretic peptide, significantly increased rat Leydig cell steroidogenesis, determining a stimulatory effect comparable to that obtained with rat atriopeptin II. Calcium-free medium and verapamil inhibited this stimulatory effect. The addition of a calcium ionophore. A-23187, significantly counteracted the inhibitory effect of verapamil on rat atriopeptin II-induced and 8-Bromoguanosine 3':5' monophosphate-induced testosterone production. Furthermore, rat atriopeptin II significantly stimulated the calcium flux through the plasma membrane, as evaluated by the 45Ca2+ uptake method. This effect was strongly inhibited by the addition of verapamil. These data underline that calcium ions may play a role in the mechanisms by which atriopeptin II stimulates rat Leydig steroidogenesis, although other post-receptor systems cannot be excluded.