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Molecular Human Reproduction, Vol. 5, No. 11, 1048-1054, November 1999
© 1999 European Society of Human Reproduction and Embryology

Molecular events in the uterus

Nitric oxide synthase expression and steroid regulation in the uterus of women with menorrhagia

S. Zervou1, L.D. Klentzeris2 and R.W. Old1,3

1 Cell and Molecular Development Group, Department of Biological Sciences, University of Warwick, Coventry CV4 7AL, and 2 Cardiff Assisted Reproduction Unit, University Hospital of Wales, Heath Park, Cardiff CF4 4XW, UK

Abstract

Menorrhagia (excessive menstrual bleeding) is a common clinical problem of unknown aetiology. The free-radical and vasodilator nitric oxide (NO) relaxes the myometrial smooth muscle and is a strong candidate for the cause of excessive blood loss in menorrhagic patients. The aim of this study was to measure NO production in women with and without menorrhagia to detect nitric oxide synthase (NOS) isoforms in uterine cells and to investigate any steroid effects on myometrial NOS expression. We showed for the first time that menorrhagic endometrium produces significantly higher amounts of NOx (the sum of NO2– and NO3–) than control endometrium (P < 0.01). Inducible NOS (iNOS) protein was detected by immunoblotting in endometrial and myometrial tissue extracts. Quantitative reverse transcription–polymerase chain reaction (RT–PCR) experiments revealed an induction of myometrial smooth muscle endothelial NOS (eNOS) expression by progesterone and 17ß-oestradiol, while myometrial iNOS expression was unaffected by steroid hormones. These results are consistent with the hypothesis that NO plays a role in excessive menstrual bleeding and provide the first evidence on steroid regulation of eNOS in the human non-pregnant uterus.

17-oestradiol/menorrhagia/nitric oxide/progesterone

Notes

3 To whom correspondence should be addressed


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