Abnormal estrous cyclicity after disruption of endothelial and inducible nitric oxide synthase in mice

Albina Jablonka-Shariff, Sapna Ravi, Angeline N. Beltsos, Laura L. Murphy, Lisa M. Olson

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Abstract

The roles of nitric oxide (NO) and nitric oxide synthase (NOS) in reproduction were studied by examining the estrous cycle of wild-type (WT) mice, inducible NOS (iNOS)-, and endothelial NOS (eNOS)-knockout mice. We observed an average estrous cycle of 4.8 ± 0.2 days in WT mice. While we observed no significant influence of iNOS deficiency on cycle length, eNOS- knockout females showed a significantly longer estrous cycle (6.6 ± 0.6 days; p < 0.03) than WT females, due to an extension of diestrus (p < 0.03). There was no influence of iNOS deficiency on ovulation rate compared with that in WT females; however, eNOS-knockout mice showed a significant reduction (p < 0.05) in ovulatory efficiency relative to WT or iNOS-knockout females. In contrast to WT females, in which the highest level of estradiol (E2) was observed at 1500 h of proestrus, iNOS-knockout females reached a peak of E2 at 1830 h of proestrus. In eNOS-knockout females, the peak of E2 occurred at 1830 h, as in iNOS-knockout mice; however, E2 levels were 5- fold and 3-fold higher (p < 0.05) than levels observed in WT and iNOS- knockout females, respectively. There was no effect of genotype on the plasma LH concentrations at proestrus. On the first day of diestrus, eNOS-knockout females showed significantly higher plasma E2 and progesterone levels (p < 0.05) relative to WT and iNOS-knockout females. The dysfunction in cyclicity, ovulation rate, ovarian morphology, and steroidogenesis in eNOS-knockout female mice strongly supports the concept that eNOS/NO plays critical roles in ovulation and follicular development.

Original languageEnglish (US)
Pages (from-to)171-177
Number of pages7
JournalBiology of reproduction
Volume61
Issue number1
DOIs
StatePublished - Jul 6 1999

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ASJC Scopus subject areas

  • Cell Biology

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