| Summary: | Background: The mechanisms for myometrial inhibition are still being investigated Aim: 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 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 registered 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 NO [Cukurova Med J 2013; 38(1.000): 92-102]
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