Immunohistochemical localization of nitric oxide synthase in the human placenta

Myatt, Leslie; Brockman, Diane E.; Eis, Annie; Pollock, Jennifer S.

doi:10.1016/s0143-4004(05)80202-4

Cited by 191 publications

(96 citation statements)

References 14 publications

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“…4A, B) immunostaining was observed mainly in syncytiotrophoblast cells and endothelial cells. Myatt et al [14,16,17], Conrad et al [15] and Buttery et al [13] reported that eNOS expression was observed in trophoblast cells in the human placenta. These findings are relevant to our present results.…”

Section: Discussionmentioning

confidence: 99%

“…Three isoforms of NOS have been identified to date, two of which are constitutively expressed as neuronal NOS (nNOS) and endothelial NOS (eNOS) requiring calcium/ calmodulin for their activity, whereas inducible NOS (iNOS) is calcium/calmodulin independent [11,12]. Biochemical experiments demonstrated the presence of eNOS in the feto-placental vasculature or dissected placental villous tissue [13][14][15][16]. However, some investigators have also provided evidence for calcium/calmodulin-independent iNOS activity in placental tissues [15,[17][18][19], although other researchers reported that iNOS mRNA expression was not detected in normal human placental tissues by RT-PCR analysis [20,21].…”

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Expression of Nitric Oxide Synthase Isoforms in the Human Placenta Is Not Altered by Labor

et al. 2003

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Abstract. Nitric oxide has various biological activities including smooth muscle relaxation, anti-inflammatory activity, anti-coagulatory activity. As the human placenta is known to express nitric oxide synthases, this study investigated the possible effect of labor on the expression of endothelial nitric oxide synthase (eNOS) and inducible nitric oxide synthase (iNOS) in human placental tissues at term. Both eNOS and iNOS mRNA expression in placental tissues in labor were significantly higher than those in the amnion, chorion laeve, decidua vera and myometrium. The eNOS mRNA and protein expressions in placental tissues in labor (n = 12) were 1.6023 ± 0.1652 (eNOS/GAPDH, mean ± SEM) and 12.8 ± 1.3 arbitrary units (AU), respectively, which were similar to those not in labor (n = 10), 1.5806 ± 0.2042 (eNOS/GAPDH) and 11.4 ± 1.8 AU. The iNOS mRNA and protein expressions in the placental tissues in labor were 1.2831 ± 0.2436 (iNOS/GAPDH) and 10.7 ± 2.1 AU respectively, similar to those not in labor, 1.9254 ± 0.8004 (iNOS/GAPDH) and 13.3 ± 1.8 AU. The guanosine 3',5'-cyclic monophosphate (cGMP) cocentration in the placental tissues in labor was 23.6 ± 1.4 fmol/g wet tissue, similar to that not in labor, 26.1 ± 2.0 fmol/g wet tissue. These findings suggest that nitric oxide production in the human placenta is maintained during labor.

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Section: Discussionmentioning

confidence: 99%

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Expression of Nitric Oxide Synthase Isoforms in the Human Placenta Is Not Altered by Labor

et al. 2003

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“…For example, increases in urinary excretion of NO metabolites and cGMP are seen in pregnant rats (49,50), and NOS activity is increased in uterine arteries from pregnant guinea pigs (48) as well as sheep (24). Furthermore, NOS expression is evident in human placental tissues (52,53). Although we observed greater than threefold increases in uterine venous and arterial levels of cGMP and a 38-fold rise in uterine cGMP production in ovine pregnancy, doses of L-NAME reaching 25 mg/ml did not consistently decrease uteroplacental blood flow even though cGMP secretion fell.…”

Section: Discussionmentioning

confidence: 99%

“…Although we observed greater than threefold increases in uterine venous and arterial levels of cGMP and a 38-fold rise in uterine cGMP production in ovine pregnancy, doses of L-NAME reaching 25 mg/ml did not consistently decrease uteroplacental blood flow even though cGMP secretion fell. It is, therefore, possible that NO does not play a primary role in maintaining basal uteroplacental blood flow in pregnant ewes, and that the placental tissues (52,53) are the predominant source of the rise in uterine venous cGMP during pregnancy. Uteroplacental prostaglandin synthesis is similarly enhanced during pregnancy (54); yet prostanoids are not solely responsible for maintaining uteroplacental perfusion (21,22).…”

Section: Discussionmentioning

confidence: 99%

Nitric oxide contributes to estrogen-induced vasodilation of the ovine uterine circulation.

Rosenfeld¹,

Cox²,

Roy³

et al. 1996

J. Clin. Invest.

204

193

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Estradiol-17 ␤ (E 2 ␤ ), a potent vasodilator, has its greatest effects on the uterine vasculature, blood flow (UBF) increasing Ն 10-fold. The mechanism(s) responsible for E 2 ␤ -induced vasodilation is unclear. We determined if nitric oxide (NO)-induced increases in cGMP modulate estrogen-induced increases in UBF, and if cyclooxygenase inhibition modifies E 2 ␤ responses. Nonpregnant ( n ϭ 15) and pregnant ( n ϭ 8) ewes had flow probes implanted on main uterine arteries and catheters in branches of the uterine vein and artery bilaterally for blood sampling and infusion of the NO synthase inhibitor L -nitro-arginine methyl ester ( L -NAME), respectively. In nonpregnant ewes E 2 ␤ (1 g/kg) caused parallel increases ( P Ͻ 0.001) in UBF (15 Ϯ 3 to 130 Ϯ 16 ml/ min) and uterine cGMP secretion (23 Ϯ 10 to 291 Ϯ 38 pmol/ min); uterine venous cGMP also rose (4.98 Ϯ 1.4 to 9.43 Ϯ 3.2 pmol/ml; P Ͻ 0.001). Intra-arterial L -NAME partially inhibited increases in UBF dose-dependently (r ϭ 0.66, n ϭ 18, P Յ 0.003) while completely inhibiting cGMP secretion ( P ϭ 0.025). Indomethacin, 2 mg/kg intravenously, did not alter E 2 ␤ -induced responses. After E 2 ␤ -induced increases in UBF, intraarterial L -NAME partially decreased UBF dose dependently (r ϭ 0.73, n ϭ 46, P Ͻ 0.001) while inhibiting cGMP secretion (178 Ϯ 48 to 50 Ϯ 24 pmol/min; n ϭ 5, P ϭ 0.006); both were reversed by L -arginine. In pregnant ewes, E 2 ␤ increased UBF and venous cGMP (9.1 Ϯ 0.96 to 13.2 Ϯ 0.96 pmol/ml, P Ͻ 0.01); however, intraarterial L -NAME decreased basal cGMP secretion 66% (P ϭ 0.02), but not UBF. Acute estrogen-induced increases in UBF are associated with NO-dependent increases in cGMP synthesis, but other mechanisms may also be involved. However, vasodilating prostanoids do not appear to be important. In ovine pregnancy NO is not essential for maintaining uteroplacental vasodilation. ( J. Clin. Invest. 1996. 98:2158-2166.)

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“…Although NOS-III was cloned originally from vascular endothelial cells (1), studies with immunohistochemical staining using specific antibodies and in situ hybridization have demonstrated NOS-III mRNA in non-endothelial cells such as human placental syncytiotrophoblasts (35) and LLC-PK1 kidney tubular epithelial cells (36). Balligand et al (37) demonstrated the expression of NOS-III in cultured rat ventricular myocytes by RT-PCR and immunohistochemistry.…”

Section: Discussionmentioning

confidence: 99%

Gene Expression of Endothelial Type Isoform of Nitric Oxide Synthase in Various Tissues of Stroke-Prone Spontaneously Hypertensive Rats.

Seki¹,

Naruse²,

Naruse³

et al. 1997

Hypertens Res

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Nitric oxide (NO) has been suggested to play important roles in the pathophysiology of various cardiovascular diseases. This study tested the hypothesis that an attenuated biological action of NO in hypertension is attributed to a change in the gene expression of NO synthase (NOS), a key enzyme involved in NO formation. The expression level of mRNA of endothelial type NOS (NOS-III) was determined in stroke-prone spontaneously hypertensive rats (SHR-SP/Izm) and Wistar Kyoto rats (WKY/Izm) by ribonuclease protection assay using a partial clone as probe. NOS-III mRNA was expressed ubiquitously in various tissues of WKY/Izm and SHR-SP/Izm either at S wk or 13 wk of age.There was no significant difference in the tissue expression of NOS-III mRNA between the two strains at either age. The intensity and localization of the hybridization signal for NOS-III mRNA in the heart of SHR-SP/Izm did not differ from those in the heart of WKY/Izm. These results suggest that the attenuated biological action of NO implied in genetically hypertensive rats is not attributed to an abnormality at the level of NOS-III mRNA expression in the tissues, although lack of an increase in NOS-III gene expression, despite the hypertensive hemodynamic stress, may modify the blood pressure in hypertension. (Hypertens Res 1997; 20: 43-49)

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Immunohistochemical localization of nitric oxide synthase in the human placenta

Cited by 191 publications

References 14 publications

Expression of Nitric Oxide Synthase Isoforms in the Human Placenta Is Not Altered by Labor

Expression of Nitric Oxide Synthase Isoforms in the Human Placenta Is Not Altered by Labor

Nitric oxide contributes to estrogen-induced vasodilation of the ovine uterine circulation.

Gene Expression of Endothelial Type Isoform of Nitric Oxide Synthase in Various Tissues of Stroke-Prone Spontaneously Hypertensive Rats.

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