Gokdeniz, RemziOvayolu, AliGarfield, Robert E.2024-08-042024-08-0420132602-30322602-3040https://hdl.handle.net/11616/103924Purpose: The mechanisms for myometrial inhibition are still being investigated. The aim of this article is to examine mechanisms of progesterone (P4) inhibition of uterine contractility. Methods: Prospective study Tertiary care center at St. Joseph's Hospital and at Maricopa Hospital, Phoenix, AZ and research center in Arizona, USA. During 2010-2011 24 women were given birth by cesarean section. Uterine tissues from women (n= 24) at term were suspended in organ chambers and exposed to various agents. Contractility was recorded and compared before and after addition of agents. Tissues were treated with P4 alone, a progestin (R5020) with low affinity to the progesterone membrane receptor (mPR), or a non-sex steroid (cholesterol). Other tissues were pretreated with inhibitors of adenylate cyclase (SQ 22536), phosphodiesterase (rolipram), nitric oxide ( NO) synthases (L-NAME) or a nuclear P4 receptor antagonist (mifepristone, MIF), followed by P4. Data were analyzed by ANOVA. Results: P4 (P< 0.05) inhibits uterine contractions. R5020 and cholesterol have little P> 0.05) inhibitory effects. P4 inhibition is not blocked by MIF, SQ, ODQ, rolipram or L-NAME ( P> 0.05). Conclusions: P4 rapidly inhibits myometrial contractility by nongenomic mechanisms through action on mPR but not via cAMP, cGMP, or NOeninfo:eu-repo/semantics/closedAccessCyclic adenosine monophosphatemyometriumpreterm laborprogesterone receptorsuterine contractilityArticle38192102WOS:000216438000012N/A