Involvement of nitric oxide pathway in prostaglandin F(2α)-induced preterm labor in rats

Y. L. Dong, Song Dai Be Song Dai, Pomila Singh, C. Yallampalli

Research output: Contribution to journalArticle

18 Citations (Scopus)

Abstract

OBJECTIVE: Our purpose was to investigate the roles of nitric oxide and prostaglandins in controlling parturition. STUDY DESIGN: Pregnant rats on day 18 of gestation were injected intraperitoneally with prostaglandin F(2α), prostaglandin F(2α) plus diethylenetriamine-nitric oxide (a donor of nitric oxide), prostaglandin F(2α) plus diethylenetriamine without nitric oxide, or vehicle. Uterine nitrite production, nitric oxide synthase messenger ribonucleic acid and contractile response in vitro, and serum progesterone levels were measured. The labor and delivery of the rats also were monitored. RESULTS: Exogenously administered prostaglandin F(2α) significantly inhibited nitric oxide production by the uterus in a time-dependent manner with maximal effects observed 48 hours after prostaglandin F(2α) treatment. Messenger ribonucleic acid for inducible nitric oxide synthase but not endothelial nitric oxide synthase messenger ribonucleic acid in the uterus was significantly inhibited by prostaglandin F(2α) with maximal inhibition at 48 hours after prostaglandin F(2α) injection. The serum progesterone concentration was substantially reduced by prostaglandin F(2α), and this reduction was partially reversed by administration of diethylenetriamine- nitric oxide but not diethylenetriamine without nitric oxide. Prostaglandin F(2α) caused increases in contractile activity of the uterus in a dose- dependent manner. Diethylenetriamine-nitric oxide (10-4 mol/L) blocked prostaglandin F(2α)-induced contractions. Premature parturition was induced within 48 hours after prostaglandin F(2α) injection in 100% of the animals. Coadministration of diethylenetriamine-nitric oxide completely prevented the preterm labor induced by prostaglandin F(2α). CONCLUSION: Prostaglandin F(2α) inhibited inducible nitric oxide synthase messenger ribonucleic acid and subsequent nitric oxide generation in the rat uterus. Nitric oxide can prevent prostaglandin F(2α)-induced preterm labor, possibly by attenuating the fall in serum progesterone and blocking uterine contractions induced by prostaglandin F(2α) administration.

Original languageEnglish (US)
Pages (from-to)907-917
Number of pages11
JournalAmerican Journal of Obstetrics and Gynecology
Volume177
Issue number4
StatePublished - 1997
Externally publishedYes

Fingerprint

Induced Labor
Premature Obstetric Labor
Prostaglandins F
Nitric Oxide
Uterus
RNA
Progesterone
Nitric Oxide Synthase Type II
Serum
Parturition
Uterine Contraction
Injections
Nitric Oxide Donors
Nitric Oxide Synthase Type III

Keywords

  • Nitric oxide
  • Preterm labor
  • Prostaglandins
  • Rat

ASJC Scopus subject areas

  • Medicine(all)
  • Obstetrics and Gynecology

Cite this

Involvement of nitric oxide pathway in prostaglandin F(2α)-induced preterm labor in rats. / Dong, Y. L.; Be Song Dai, Song Dai; Singh, Pomila; Yallampalli, C.

In: American Journal of Obstetrics and Gynecology, Vol. 177, No. 4, 1997, p. 907-917.

Research output: Contribution to journalArticle

Dong, Y. L. ; Be Song Dai, Song Dai ; Singh, Pomila ; Yallampalli, C. / Involvement of nitric oxide pathway in prostaglandin F(2α)-induced preterm labor in rats. In: American Journal of Obstetrics and Gynecology. 1997 ; Vol. 177, No. 4. pp. 907-917.
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AU - Dong, Y. L.

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AU - Singh, Pomila

AU - Yallampalli, C.

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N2 - OBJECTIVE: Our purpose was to investigate the roles of nitric oxide and prostaglandins in controlling parturition. STUDY DESIGN: Pregnant rats on day 18 of gestation were injected intraperitoneally with prostaglandin F(2α), prostaglandin F(2α) plus diethylenetriamine-nitric oxide (a donor of nitric oxide), prostaglandin F(2α) plus diethylenetriamine without nitric oxide, or vehicle. Uterine nitrite production, nitric oxide synthase messenger ribonucleic acid and contractile response in vitro, and serum progesterone levels were measured. The labor and delivery of the rats also were monitored. RESULTS: Exogenously administered prostaglandin F(2α) significantly inhibited nitric oxide production by the uterus in a time-dependent manner with maximal effects observed 48 hours after prostaglandin F(2α) treatment. Messenger ribonucleic acid for inducible nitric oxide synthase but not endothelial nitric oxide synthase messenger ribonucleic acid in the uterus was significantly inhibited by prostaglandin F(2α) with maximal inhibition at 48 hours after prostaglandin F(2α) injection. The serum progesterone concentration was substantially reduced by prostaglandin F(2α), and this reduction was partially reversed by administration of diethylenetriamine- nitric oxide but not diethylenetriamine without nitric oxide. Prostaglandin F(2α) caused increases in contractile activity of the uterus in a dose- dependent manner. Diethylenetriamine-nitric oxide (10-4 mol/L) blocked prostaglandin F(2α)-induced contractions. Premature parturition was induced within 48 hours after prostaglandin F(2α) injection in 100% of the animals. Coadministration of diethylenetriamine-nitric oxide completely prevented the preterm labor induced by prostaglandin F(2α). CONCLUSION: Prostaglandin F(2α) inhibited inducible nitric oxide synthase messenger ribonucleic acid and subsequent nitric oxide generation in the rat uterus. Nitric oxide can prevent prostaglandin F(2α)-induced preterm labor, possibly by attenuating the fall in serum progesterone and blocking uterine contractions induced by prostaglandin F(2α) administration.

AB - OBJECTIVE: Our purpose was to investigate the roles of nitric oxide and prostaglandins in controlling parturition. STUDY DESIGN: Pregnant rats on day 18 of gestation were injected intraperitoneally with prostaglandin F(2α), prostaglandin F(2α) plus diethylenetriamine-nitric oxide (a donor of nitric oxide), prostaglandin F(2α) plus diethylenetriamine without nitric oxide, or vehicle. Uterine nitrite production, nitric oxide synthase messenger ribonucleic acid and contractile response in vitro, and serum progesterone levels were measured. The labor and delivery of the rats also were monitored. RESULTS: Exogenously administered prostaglandin F(2α) significantly inhibited nitric oxide production by the uterus in a time-dependent manner with maximal effects observed 48 hours after prostaglandin F(2α) treatment. Messenger ribonucleic acid for inducible nitric oxide synthase but not endothelial nitric oxide synthase messenger ribonucleic acid in the uterus was significantly inhibited by prostaglandin F(2α) with maximal inhibition at 48 hours after prostaglandin F(2α) injection. The serum progesterone concentration was substantially reduced by prostaglandin F(2α), and this reduction was partially reversed by administration of diethylenetriamine- nitric oxide but not diethylenetriamine without nitric oxide. Prostaglandin F(2α) caused increases in contractile activity of the uterus in a dose- dependent manner. Diethylenetriamine-nitric oxide (10-4 mol/L) blocked prostaglandin F(2α)-induced contractions. Premature parturition was induced within 48 hours after prostaglandin F(2α) injection in 100% of the animals. Coadministration of diethylenetriamine-nitric oxide completely prevented the preterm labor induced by prostaglandin F(2α). CONCLUSION: Prostaglandin F(2α) inhibited inducible nitric oxide synthase messenger ribonucleic acid and subsequent nitric oxide generation in the rat uterus. Nitric oxide can prevent prostaglandin F(2α)-induced preterm labor, possibly by attenuating the fall in serum progesterone and blocking uterine contractions induced by prostaglandin F(2α) administration.

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