Endocrine regulation and communicating functions of the Leydig cell.

摘要: Activation and regulation of Leydig cell function is exerted primarily by LH, which secreted in pulses high biological activity interacts with membrane receptors. Other hormones factors the or from tubular compartment can influence differentiation acute chronic actions LH on steroidogenesis. Conversely, produced could modulate (e.g. beta-endorphin, oxcytocin). The receptor has been purified to homogeneity sufficient quantities allow its peptide sequence be determined gene structure elucidated as well functional reconstitution studies performed. subunit Mr 90,000 phosphorylated cAMP-dependent protein kinase. native appears exist a dimer identical subunits associated noncovalent interactions. It likely that dimerization further aggregation are necessary for signal transduction occur, phosphorylation one more kinases may involved regulating gonadotropin action. Stimulation androgen pathway occurs mainly through cAMP-mediated mechanism. stimulatory event negatively influenced action certain guanyl nucleotide inhibitory adenylate cyclase. Such an angiotensin emphasized importance cAMP cell. hormone also facilitate production cAMP-independent mechanism located at plasma intracellular sites. A Ca2+ sensitive kinase system present membranes. presence nM amounts induces 45,000. Adenylate cyclase activation affected Ca2+. Membrane modifier LH-stimulated possibly other LH-induced activated membrane. In adult rat testis, ability cells respond sustained gonadotropic stimulation increased limited development refractory state loss receptors steroidogenic enzymes. Gonadotropin-induced lesions testes include late lesion site conversion progesterone early before pregnenolone formation leads decreased vitro testosterone response hCG.