Multistep regulation of Leydig cell function.

摘要: LH controls Leydig cell steroidogenesis by interaction with specific membrane receptors initiating coupling events. Stimulation of the androgen pathways occurs mainly through cAMP mediated mechanism including induced guanyl nucleotide binding, phosphorylation and adenylate cyclase activation. dependent kinase activation presumably causes key proteins steroidogenic pathway consequent increase in testosterone production. The hormone also appears to facilitate stimulus a cyclic AMP independent located at plasma or intracellular sites. stimulatory event can be negatively influenced action certain peptide hormones (i.e. angiotensin II) inhibitory subunit (Gi). In recent studies we have presented evidence for Ca2+ sensitive system present purified membranes. Gpp(NH)p, GTP, phospholipid presence nanomolar induce phosphate incorporation into Mr 44,500 substrate marked inhibition microM Ca2+. Similarly biphasic pattern was observed activity. Membrane may modifier LH-stimulated activity possibly other actions activated membrane. Furthermore defined effects forskolin on all pools provided additional functional compartmentalization and/or facilitory trophic hormone. demonstration novel high affinity upon generation Gi has new approach direct evaluation influence cell. cultured fetal useful model elucidate mechanisms involved development gonadotropin estradiol desensitization steroidogenesis. We isolated from testis small population (2-5% total) transitional cells morphological characteristics found 15 day postnatal but capabilities adult demonstrated after appropriate treatment estrogen, frequent dose) emergence adult-like type population.