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

Abstract

Foresta C, Mioni R. The role of calcium ions in rat Leydig cell steroidogenesis induced by atrial natriuretic peptide. Acta Endocrinol 1993:128:274-80. ISSN 0001-5598 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 Il-treated rat Leydig cells. Similar effects were observed on human chorionic gonadotropin-stimulated Leydig cells. Furthermore, 8-Bromoguanosine 3\m=' \:5\m=' \cyclic mono\x=req-\ phosphate, 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 I I \ x=r eq-\ induced and 8-Bromoguanosine 3\ m=' \ : 5\ m=' \ 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.

Inhibition of testosterone secretion by digitoxin in rat testicular interstitial cells

“…Our results indicated that digitoxin have the inhibitory effect on the testicular function both in vivo and in vitro. This effect may partly result from the increased secretion of atrial natriuretic peptide (ANP) from atrial myocytes, and ANP can exert a potent direct inhibitory effect on testicular function [Mukhopadhyay et al, 1986;Foresta et al, 1993]. In addition, this study showed that digitoxin can act directly on the testicular interstitial cells to inhibit the secretion of testosterone (Fig.…”

Inhibitory effect of digoxin on testosterone secretion through mechanisms involving decreases of cyclic AMP production and cytochrome P450scc activity in rat testicular interstitial cells

“…An early study suggested that long-term digoxin therapy may also depress LH secretion by the pituitary gland (Tappler & Katz, 1979), a phenomenon which would be expected to exacerbate the direct inhibitory actions of the drug on testicular testosterone secretion. Similarly, the digoxininduced blockade of testosterone synthesis in vivo may be reinforced by the concomitant fall of atrial natriuretic peptide (ANP), a peptide which stimulates testosterone secretion in vitro in a time and concentration-dependent manner (Mukhopadhyay et al, 1986;Foresta & Mioni, 1993).…”

Erythropoietin and testicular steroidogenesis: the role of second messengers

“…Early studies of the mechanism of action of erythropoietin addressed the possibility that cyclic nucleotides might serve as second messengers (18,19). It is well known that in rat Leydig cells both cAMP and cGMP are involved as second messengers in the steroidogenetic effect of agonists such as hCG and atrial natriuretic peptide (ANP) (21), [26][27][28][29]. However, the absence of any variation of cAMP and cGMP levels after rHuEPO treatment observed in this study suggests that in rat Leydig cells the affect of EPO, as well as of GnRH, does not involve adenylate or guanylate-cyclase systems.…”