Analysis of Nitric Oxide Metabolism as a Placental or Maternal Factor Underlying the Etiology of Pre-Eclampsia
In: Gynecologic and obstetric investigation, Jg. 68 (2009), Heft 4, S. 239-247
Online
academicJournal
- print, 22 ref
Zugriff:
Background: Defective nitric oxide (NO)-mediated vasodilation is widely regarded as an underlying cause of hypertension in pre-eclampsia, although there are also arguments against this hypothesis. Methods: We examined both the mRNA levels and the presence of a Glu298Asp substitution in the NO synthase (NOS) gene, as well as the NO metabolite concentration, in placentas and maternal sera from women with pre-eclampsia and in normotensive pregnant controls (25-40 vs. 24-41 weeks of gestation). Results: Pre-eclamptic and control placentas did not show any significant differences in their NO metabolite levels or their NOS expression levels as measured by quantitative RT-PCR. In addition, we did not find any association between pre-eclampsia and the occurrence of the Glu298Asp amino acid substitution in the NOS gene. In contrast, high maternal circulating NO metabolites were evident in severe pre-eclampsia (p < 0.0001). Although a positive correlation between circulating NO metabolites and blood pressure was not observed, uterine artery resistance measured by ultrasound was found to positively correlate with the maternal NO levels. Conclusions: Ourcurrentdata suggest that an altered placental NOS pathway is unlikely to be the primary cause of pre-eclampsia and that the activation of this pathway is possibly in response to maternal symptoms.
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Analysis of Nitric Oxide Metabolism as a Placental or Maternal Factor Underlying the Etiology of Pre-Eclampsia
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Autor/in / Beteiligte Person: | NISHIZAWA, Haruki ; PRYOR-KOISHI, Kanako ; SUZUKI, Machiko ; KATO, Takema ; SEKIYA, Takao ; TADA, Shin ; KURAHASHI, Hiroki ; UDAGAWA, Yasuhiro |
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Zeitschrift: | Gynecologic and obstetric investigation, Jg. 68 (2009), Heft 4, S. 239-247 |
Veröffentlichung: | Basel: Karger, 2009 |
Medientyp: | academicJournal |
Umfang: | print, 22 ref |
ISSN: | 0378-7346 (print) |
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