Nitric Oxide Synthase Activity in the Pregnant Uterus Decreases at Parturition

Natuzzi, Eileen; Ursell, Philip C.; Harrison, Michael R.; Buscher, C.; Riemer, R. Kirk

doi:10.1006/bbrc.1993.1776

Cited by 142 publications

(91 citation statements)

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“…Timed pregnant rats (Holtzman, Harlan Sprague-Dawley) were obtained on gestational d 6 of a 22-d gestation. They were randomly assigned to one of three treatment groups: the first received the NOS inhibitor, L-NAME (Sigma Chemical Co., St. Louis, MO) at 0.3 or 1.0 mg/mL in the drinking water, for 14 prenatal days (gestational d [6][7][8][9][10][11][12][13][14][15][16][17][18][19]. Based on water consumpti on these doses of L-NAME approximate to 55 and 180 mg/kg/day, respectively.…”

Section: Prenatal Studiesmentioning

confidence: 99%

“…Th e uteroplacental unit via both co nst itutive and inducible pathways appea rs to form NO und er these co nd itions (11,12). We recently reported that earl y third trimest er (gestation al d [13][14][15][16][17][18][19] NOS inhibition with I.-NA ME in rats, alth ough not affecting indices of maternal health, resulted in mark ed fetal and placent al grow th retardation (13) .…”

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confidence: 99%

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Perinatal Nitric Oxide Synthase Inhibition Retards Neonatal Growth by Inducing Hypertrophic Pyloric Stenosis in Rats

et al. 1995

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Administration of the nitric oxide synthase (NOS) inhibitor, AP-nitro-L-arginine methyl ester (L-NAME) during pregnancy has been shown to compromise fetal growth. This study was designed to determine whether aminoguanidine, a predominate inhibitor of inducible NOS, affects fetal outcome. In addition, we extended the prenatal administration of L-NAME into the postnatal period (14 d) to determine whether neonatal growth and maturation were also affected. L-NAME, but not aminoguanidine, compromises fetal and placental growth. When compared with control 14-d-old pups, postnatal L-NAMEcompromised neonatal growth, whether it was given directly (intraperitoneally) (39.7 ± 1.1 versus 24.1 ± 1.0 g) or indirectly (38.6 ± 0.5 versus 22.2 ± 1.2 g) via maternal breast milk. Neonatal growth retardation was asymmetric, with brain sparing, suggesting a nutritional origin. L-NAME administration resulted in growth retardation that extended into adulthood, without evidence of catch-up growth. Treated neonates displayed the hallmarks of hypertrophic pyloric stenosis. Significant increases in stomach weight/pup weight (9.9 ± 0.3 versus 8.2 ± 0.4 X 10 3 ) and stomach volume/pup weight (12.0 ± 0.6 versus 9.4 ± 0.6 mL/100 g) with a concomitant Endogenous NO produced from L-arginine by NOS (1), is an important regulator in a number of physiologic proce sse s. Se veral different isoforms of NOS exist; the con stitutive isoforms regul ate v ascular tone (1), neurotransmission (2), and platelet aggregation (3), w hereas the ind ucible for m appears to have its primary effect s on inflammation (4, 5) and host defense (6). A number of exog enous NOS inhibitors have been identified including the structural an alog of L-arginine, I.-NA ME, w hich inhibits both co nstitutive and inducible NOS isoforms , wi th pr eference for the constitut ive isoform (7,8 Supported in parI by National Institutes of Health Granl ROI HD31885 (to MJ.S.M.) and American Heart Association, Louisiana Chapter (to M.R.P.). decrease in small intestine weight/length (2.10 ± 0.08 versus 3.18 ± 0.13 g/100 em) was noted in treated versus control pups (p < 0.05). Muscularis hypertrophy at the pyloric sphincter in the L-NAME-treated pups was noted by histology. Blood pressure was elevated in the L-NAME-treated pups (93 ± 6 versus 60 ± 5 mm Hg in control pups, p < 0.05). These findings are consistent with inhibition of neuronal and endothelial NOS activity. We conclude that NO, formed via the constitutive isoforms of NOS, is a critical determinant of fetal and neonatal growth and maturation. (Pediatr Res 38: 768-774, 1995) Abbreviations NO, nitric oxide NOS, nitric oxide synthase cNOS, constitutive nitric oxide synthase iNOS, inducible nitric oxide synthase L-NAME, AP-nitro-L-arginine methyl ester HPS , hypertrophic pyloric stenosis VIP , vasoactive intestinal polypeptide nidine, although not a i-arginine anal og, predominately inhibits the indu cible NOS isoform (9) .NO fo rma tion is up-regul ated in pregn ancy (10). Th e uteroplacental unit via both co nst itutive and ind...

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Section: Prenatal Studiesmentioning

confidence: 99%

mentioning

confidence: 99%

Perinatal Nitric Oxide Synthase Inhibition Retards Neonatal Growth by Inducing Hypertrophic Pyloric Stenosis in Rats

et al. 1995

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“…Our group and other researchers have demonstrated that NO is produced by a variety of uterine cell types, including endometrial epithelium, metrial glands, decidua, myometrial cells, NK cells, and macrophages (6,7,28,38,40). Previous work has also implicated NO as a modulator of uterine infection, including the finding that NO inhibition increased the lethality of experimental intrauterine infection in pregnant rats and that intrauterine infection results in a localized increase in NO synthesis (9,30).…”

Section: Discussionmentioning

confidence: 74%

Epithelial Invasion by Escherichia coli Bearing Dr Fimbriae Is Controlled by Nitric Oxide-Regulated Expression of CD55

Li¹,

Nowicki

Urvil³

et al. 2004

Infect Immun

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We previously reported that inhibition of nitric oxide (NO) increases the rate of bacteremia and maternal mortality in pregnant rats with uterine infection by Escherichia coli expressing the Dr fimbria (Dr ؉ ). Epithelial binding and invasion by Dr ؉ E. coli has also been shown to be dependent upon the expression level of the cellular receptor decay-accelerating factor (DAF; CD55). Here, we hypothesize that NO-related severity of infection could be mediated by changes in DAF expression and in the rate of epithelial invasion. The cellular basis of NO effects on epithelial invasion with Dr ؉ E. coli was studied using Ishikawa endometrial carcinoma cells as an in vitro model of the human endometrial epithelium. Initially, we show that Ishikawa cells produce NO and express both NO synthase enzymes, NOS II and NOS III, and DAF protein. We next tested the abilities of both Dr ؉ E. coli and a Dr ؊ E. coli mutant to invade Ishikawa cells, and invasion was seen only with Dr ؉ E. coli. Invasion by Dr ؉ E. coli was decreased by elevated NO production and increased by NO inhibition. Elevated NO production significantly decreased DAF protein and mRNA expression in Ishikawa cells in a time-and dose-dependent manner. Here, we propose that in vitro invasion of an epithelial cell line is directly related to NO-regulated expression of DAF. The significance of NO-regulated receptor-ligand invasion is that it may represent a novel unrecognized phenomenon of epithelial defense against infection.Although urogenital microbial infection in pregnancy is an important cause of maternal and neonatal morbidity and mortality, the mechanisms of defense against gestational intrauterine infection are poorly understood (8,14,23). Evidence obtained in studies of both humans and rats suggests that the bacteriostatic actions of nitric oxide (NO) are an important component of defense against urogenital infection (16,30,33). Nitric oxide is synthesized in situ from an L-arginine substrate by one or more of three NO synthase isoforms (NOS I, NOS II, and NOS III), each of which has been identified in the mouse, rat, and human (1,27,40,41).Several lines of evidence have demonstrated the involvement of intracellular NO in the host defense mechanisms against bacterial infections (5, 27). Recently, NO production and three NOS isoforms were reported to be present in rat uterine tissues, and elevated NOS II expression was demonstrated to contribute to the increased NO production in the rat uterus and consequent uterine quiescence during gestation (3, 4, 40). However, the role of the NO system in uterine defense mechanisms is not well understood.Three separate lines of evidence from our laboratories have suggested that increased NO production by the urogenital tract in pregnancy protects against Escherichia coli infection. First, inhibition of NO synthesis in pregnant rats with an intrauterine infection increases maternal death (30). Second, the sensitivity of the female rat or mouse urinary tract to E. coli infection was increased with inhibition of NO (30,3...

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“…In the years 1994-1996 378,100 women with pelvic/abdominal pain underwent ambulatory diagnostic laparoscopy for pelvic pain. This figure excluded women undergoing laparoscopy as an in-patient procedure and represents 34% of the 1.1 million diagnostic laparoscopies performed in the U.S. during that period (Natuzzi et al, 1993). One-third of all diagnostic laparoscopies revealed endometriosis, one-third revealed no visible pathology, and the remaining one-third demonstrated a variety of other gynecologic conditions (Howard, 1993).…”

Section: Fig 1 Laparosocpymentioning

confidence: 99%

Laparoscopy for Diagnosis and Treatment of Endometriosis

Al-Jefout¹

2011

Advanced Gynecologic Endoscopy

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Nitric Oxide Synthase Activity in the Pregnant Uterus Decreases at Parturition

Cited by 142 publications

References 0 publications

Perinatal Nitric Oxide Synthase Inhibition Retards Neonatal Growth by Inducing Hypertrophic Pyloric Stenosis in Rats

Perinatal Nitric Oxide Synthase Inhibition Retards Neonatal Growth by Inducing Hypertrophic Pyloric Stenosis in Rats

Epithelial Invasion by Escherichia coli Bearing Dr Fimbriae Is Controlled by Nitric Oxide-Regulated Expression of CD55

Laparoscopy for Diagnosis and Treatment of Endometriosis

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