Altered mRNA expression of ecNOS and iNOS in myometrium and placenta from women with preeclampsia

Faxén, Margareta; Nisell, Henry; Kublickiene, K

doi:10.1007/s004040000152

Cited by 33 publications

(20 citation statements)

References 36 publications

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“…Endothelium-derived NO is upregulated in the uterine vascular bed in the pregnancy of most species (8,44,46); thus it might contribute to the regulation of MT in MA in pregnancy (9,19). Notably, NOS inhibition increased MT in MA from pregnant but not nonpregnant women; thus, NO appears to modulate myogenic responses in MA during pregnancy.…”

Section: Discussionmentioning

confidence: 91%

Pregnancy increases myometrial artery myogenic tone via NOS- or COX-independent mechanisms

Eckman

Gupta

Rosenfeld

et al. 2012

American Journal of Physiology-Regulatory, Integrative and Comp

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Myogenic tone (MT) is a primary modulator of blood flow in the resistance vasculature of the brain, kidney, skeletal muscle, and perhaps in other high-flow organs such as the pregnant uterus. MT is known to be regulated by endothelium-derived factors, including products of the nitric oxide synthase (NOS) and/or the cyclooxygenase (COX) pathways. We asked whether pregnancy influenced MT in myometrial arteries (MA), and if so, whether such an effect could be attributed to alterations in NOS and/or COX. MA (200-300 μm internal diameter, 2-3 mm length) were isolated from 10 nonpregnant and 12 pregnant women undergoing elective hysterectomy or cesarean section, respectively. In the absence of NOS and/or COX inhibition, pregnancy was associated with increased MT in endothelium-intact MA compared with MA from nonpregnant women (P < 0.01). The increase in MT was not due to increased Ca(2+) entry via voltage-dependent channels since both groups of MA exhibited similar levels of constriction when exposed to 50 mM KCl. NOS inhibition (N(ω)-nitro-L-arginine methyl ester, L-NAME) or combined NOS/COX inhibition (L-NAME/indomethacin) increased MT in MA from pregnant women (P = 0.001 and P = 0.042, respectively) but was without effect in arteries from nonpregnant women. Indomethacin alone was without effect on MT in MA from either nonpregnant or pregnant women. We concluded that MT increases in MA during human pregnancy and that this effect was partially opposed by enhanced NOS activity.

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Section: Discussionmentioning

confidence: 91%

Pregnancy increases myometrial artery myogenic tone via NOS- or COX-independent mechanisms

Eckman

Gupta

Rosenfeld

et al. 2012

American Journal of Physiology-Regulatory, Integrative and Comp

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“…NO is a potent vasodilator and is generated by the catalytic action of NO synthases endothelial NOS (eNOS) and inducible NOS (iNOS) in myometrium and placenta. 2 Various studies have been conducted for iNOS mRNA expression in PE but the results are conflicting. 3,4 The release of NO in the presence of iNOS can be influenced by complex signalling mechanisms.…”

Section: Introductionmentioning

confidence: 98%

Inducible nitric oxide synthase (iNOS) gene polymorphism in pre‐eclampsia: A pilot study in North India

Bhatnagar¹,

Bhattacharjee²,

Vaid

et al. 2007

Aust NZ J Obst Gynaeco

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“…Interestingly, umbilical vein smooth muscle cells seem to express nNOS mRNA (the levels of which are significantly reduced in preeclamptic pregnancies and parallel the lack of nNOS protein) [187]. Early results show iNOS expression in the placental microvascular endothelium [163]. This contrasts with the reduced iNOS expression reported in total protein extracts from placenta [163,188] and in cultured trophoblasts [185].…”

Section: Cationic Amino Acid Transportmentioning

confidence: 84%

“…To date, higher levels of nitrites and nitrates have been reported in umbilical vein blood [157,158], amniotic liquid [159] and in the supernatant of primary cultures of HUVEC [160]. In addition, it has been shown that umbilical veins are more susceptible to relaxation induced by NO through an increased synthesis of cGMP [161], and that placental homogenates exhibit higher synthesis of L-[ 3 H]citrulline from L-[ 3 H]arginine [162,163] in preeclampsia. These observations could reflect compensatory mechanisms to ameliorate the effects of preeclampsia on the foetal-placental vasculature.…”

Section: Cationic Amino Acid Transportmentioning

confidence: 96%

Equilibrative Nucleoside (ENTs) and Cationic Amino Acid (CATs) Transporters: Implications in Foetal Endothelial Dysfunction in Human Pregnancy Diseases

Casanello¹,

Escudero²,

Sobrevía

2007

CVP

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Gestational diabetes (GD, characterized by abnormal D-glucose metabolism), intrauterine growth restriction (IUGR, a disease associated with reduced oxygen delivery (hypoxia) to the foetus), and preeclampsia (PE, a pregnancy complication characterized by high blood pressure, proteinuria and increased vascular resistance), induce foetal endothelial dysfunction with implications in adult life and increase the risk of vascular diseases. Synthesis of nitric oxide (NO) and uptake of L-arginine (the NO synthase (NOS) substrate) and adenosine (a vasoactive endogenous nucleoside) by the umbilical vein endothelium is altered in pregnancies with GD, IUGR or PE. Mechanisms underlying these alterations include differential expression of equilibrative nucleoside transporters (ENTs), cationic amino acid transporters (CATs), and NOS. Modulation of ENTs, CATs, and NOS expression and activity in endothelium involves protein kinase C (PKC), mitogen-activated protein kinases p42 and p44 (p42/44(mapk)), calcium, and phosphatidyl inositol 3 kinase (PI3k), among others. Elevated extracellular D-glucose and hypoxia alter human endothelial function. However, information regarding the transcriptional modulation of ENTs, CATs, and NOS is limited. This review focuses on the effect of transcriptional and post-transcriptional regulatory mechanisms involved in the modulation of ENTs and CATs, and NOS expression and activity, and the consequences for foetal endothelial function in GD, IUGR and PE. The available information will contribute to a better understanding of the cell and molecular basis of the altered vascular endothelial function in these pregnancy diseases and will emphasize the key role of this type of epithelium in placental function and the normal foetal development and growth.

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Altered mRNA expression of ecNOS and iNOS in myometrium and placenta from women with preeclampsia

Cited by 33 publications

References 36 publications

Pregnancy increases myometrial artery myogenic tone via NOS- or COX-independent mechanisms

Pregnancy increases myometrial artery myogenic tone via NOS- or COX-independent mechanisms

Inducible nitric oxide synthase (iNOS) gene polymorphism in pre‐eclampsia: A pilot study in North India

Equilibrative Nucleoside (ENTs) and Cationic Amino Acid (CATs) Transporters: Implications in Foetal Endothelial Dysfunction in Human Pregnancy Diseases

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