HomeHypertensionVol. 50, No. 5Response to Preeclamptic Superoxide-Anion Production: Is There an Increase or a Failure of Reduction? Free AccessLetterPDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessLetterPDF/EPUBResponse to Preeclamptic Superoxide-Anion Production: Is There an Increase or a Failure of Reduction? Kiyomi Tsukimori, Hitoo Nakano and Norio Wake Kiyomi TsukimoriKiyomi Tsukimori Department of Obstetrics and Gynecology, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan Search for more papers by this author , Hitoo NakanoHitoo Nakano Department of Obstetrics and Gynecology, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan Search for more papers by this author and Norio WakeNorio Wake Department of Obstetrics and Gynecology, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan Search for more papers by this author Originally published24 Sep 2007https://doi.org/10.1161/HYPERTENSIONAHA.107.100412Hypertension. 2007;50:e168–e164Other version(s) of this articleYou are viewing the most recent version of this article. Previous versions: September 24, 2007: Previous Version 1 We thank Lampé et al1 for their interest in our article.2 These investigators have highlighted the fact that granulocyte superoxide-anion (O2−) production is decreased in normal pregnancy, whereas preeclampsia is associated with failure of this reduction of O2− production.We have previously studied O2− production in neutrophils from 78 normal pregnant women at 7 to 39 weeks of gestation to determine whether there is a critical gestational age at which maternal neutrophil O2− production occurs.3 In this report, we demonstrated that n-formyl-methionyl-leucyl-phenylalanine–induced O2− production is significantly increased in normal pregnancy, particularly during the early second trimester (19 to 22 weeks of gestation). Other investigators have also reported that the level of intracellular leukocyte reactive oxygen species is significantly increased during normal pregnancy and is further increased in women with preeclampsia, but by 6 weeks postpartum, intracellular leukocyte reactive oxygen species levels return to normal nonpregnancy levels in both groups of women.4 The above observations appear to contradict the claims of Lampé et al1 that neutrophil O2− production is decreased in normal pregnancy.Although we indeed used HEPES buffer in our article,2 we measured neutrophil O2− production immediately after preparation of the neutrophils, whereas only our investigation of the effect of sera from patients with preeclampsia on O2− production of neutrophils from nonpregnant women involved a 1-hour incubation at 37°C. In addition, we have reported previously that any serum-enhancing effects on neutrophil O2− production in women with preeclampsia did not promote mobilization of intracellular calcium ions.5 Thus, the observed differences between the study groups in our report were intrinsic to the groups rather than related to the methods. Furthermore, we have reported previously that, when neutrophils are stimulated by phorbol ester, neutrophil O2− production in women with preeclampsia did not differ significantly from that in normal pregnant women or that in normal nonpregnant women, suggesting that the enhanced neutrophil O2− production in women with preeclampsia might be achieved via modulation of the O2− production signal transduction pathway between n-formyl-methionyl-leucyl-phenylalanine receptors and protein kinase C.5We welcome suggestions regarding the mechanisms of increased neutrophil O2− production in women with preeclampsia. Our article suggests that serum factors play a more essential role in O2− production than does neutrophil behavior, ie, women with preeclampsia possess a genetic predisposition toward increased neutrophil O2− production.2 Potential neutrophil stimulants in preeclampsia include proinflammatory cytokines and exportation of syncytiotrophoblast microvesicles, both of which result from damage to the placenta. Thus, placental ischemia may be important in initiating the systemic neutrophil activation observed in preeclampsia.DisclosuresNone.1 Lampé R, Szűcs S, Adány R, Póka R. Preeclamptic superoxide-anion production: is there an increase or a failure of reduction? Hypertension. 2007; 50: e167.LinkGoogle Scholar2 Tsukimori K, Nakano H, Wake N. Difference in neutrophil superoxide generation during pregnancy between preeclampsia and essential hypertension. Hypertension. 2007; 49: 1436–1441.LinkGoogle Scholar3 Ishida K, Tsukimori K, Nagata H, Koyanagi T, Akazawa K, Nakano H. Is there a critical gestational age in neutrophil superoxide production activity? Blood. 1995; 85: 1331–1333.CrossrefMedlineGoogle Scholar4 Sacks GP, Studena K, Sargent IL, Redman CWG. Normal pregnancy and preeclampsia both produce inflammatory changes in peripheral blood leukocytes akin to those of sepsis. Am J Obstet Gynecol. 1998; 179: 80–86.CrossrefMedlineGoogle Scholar5 Tsukimori K, Maeda H, Ishida K, Nagata H, Koyanagi T, Nakano H. The superoxide generation of neutrophils in normal and preeclamptic pregnancies. Obstet Gynecol. 1993; 81: 536–540.MedlineGoogle Scholar Previous Back to top Next FiguresReferencesRelatedDetails November 2007Vol 50, Issue 5 Advertisement Article InformationMetrics https://doi.org/10.1161/HYPERTENSIONAHA.107.100412 Originally publishedSeptember 24, 2007 PDF download Advertisement SubjectsHypertension