Luteolytic hormones are calcium-mediated, guanine nucleotide antagonists of gonadotropin-sensitive adenylate cyclase.
We suggest that regression of the corpus luteum is an active process induced by PGF2 alpha, GnRH, and a peptide of ovarian origin whose action GnRH mimics (20). The initial events involved in luteolysis occur within minutes, and they are intimately linked to inhibition of LH action. Membrane receptor binding of luteolytic hormones activates production of a second messenger (such as a product of PI turnover) that stimulates release of sequestered, intracellular Ca2+ by a mechanism linked to inhibition of microsomal Ca2+-ATPase activity. The increase in cytosolic Ca2+ inhibits adenylate cyclase activity by blocking GTP-dependent activation of adenylate cyclase. As a result, the cell response to LH is abolished and function is lost.
D000262:Adenylyl Cyclases / Q000378:metabolism*; D000818:Animals; D002118:Calcium / Q000494:pharmacology*; D003338:Corpus Luteum / Q000187:drug effects / Q000502:physiology*; D015237:Dinoprost; D005260:Female; D006150:Guanine Nucleotides / Q000494:pharmacology*; D007986:Luteinizing Hormone / Q000494:pharmacology*; D011460:Prostaglandins F / Q000494:pharmacology*
D006150:Guanine Nucleotides; D011460:Prostaglandins F; D007986:Luteinizing Hormone; D015237:Dinoprost; D000262:Adenylyl Cyclases; D002118:Calcium