Modulation of K+ conductances by Ca2+ and human chorionic gonadotrophin in Leydig cells from mature rat testis

1. Although the control of steroidogenic activity of the Leydig cell by the peptides luteinizing hormone (LH) and human chorionic gonadotrophin (hCG) is clearly mediated by cAMP, the extent to which Ca2+ controls the Leydig cell function is less well defined. In the present study, the whole-cell configuration of the patch-clamp technique was used to investigate the modulation of potassium conductances by calcium and hCG, in the Leydig cells from mature rat testis. 2. In symmetrical glutamate solutions, depolarizations elicited outwardly rectifying currents, which were mainly carried by potassium and were blocked by tetraethylammonium and 4-aminopyridine. For values of [Ca2+]i below 10(-8) M, transient currents of low amplitudes, insensitive to charybdotoxin (CTX) and iberiotoxin (IBTX), were activated above -40 mV. For [Ca2+]i values of 10(-7) M and above, noisy currents with slow activation kinetics were activated above 0 mV. These currents were sustained and were sensitive to CTX and IBTX. 3. Both current types were modulated by intracellular calcium. Ionomycin and a [Ca2+]i elevation in the range from 10(-9) to 10(-7) M, both inhibited the CTX-insensitive currents, whereas a rise in the calcium concentration above 10(-7) M increased the amplitude and shifted the threshold of activation of the CTX-sensitive currents to less positive levels. 4. hCG (1-50 i.u. ml-1), in conditions where the chloride currents were strongly inhibited by 4-acetamido-4'-isothiocyanatostilbene-2,2'-disulphonic acid (SITS), induced a partial inhibition of the CTX-insensitive currents but was unable to increase the CTX-sensitive currents. 5. No voltage-sensitive calcium current was recorded in control or hCG-stimulated cells. 6. The results indicate that hCG inhibits one kind of Ca(2+)-modulated channel, perhaps as a result of a moderate [Ca2+]i rise, but is unable to increase the intracellular Ca2+ concentration to the range in which large conductance Ca(2+)-dependent channels are activated.