Pregnancy-induced alterations of neurogenic constriction and dilation of human uterine artery

Nelson, Sharon H.; Steinsland, Odd S.; Johnson, Rebecca L.; Suresh, S.; Gifford, Andrew N.; Ehardt, J. S.

doi:10.1152/ajpheart.1995.268.4.h1694

Cited by 27 publications

(33 citation statements)

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“…Atropine, ␤-adrenoceptor antagonists, indomethacin, and endothelium-denudation failed to inhibit the response, which was however abolished by oxyHb. The neurogenic, NO-mediated relaxation was greater in the uterine artery from pregnant patients undergoing hysterectomy than that from nonpregnant patients (Nelson et al, 1995b). In the guinea pig artery, high frequency stimulation (Ͼ5 Hz) also liberates vasodilator peptides (Morris, 1993), but this does not seem to be the case in the other mammals.…”

Section: E Uterine Vasculaturementioning

confidence: 90%

“…As described formerly, NO derived from vascular endothelium is not the sole endogenous NO participating in circulatory homeostasis. The presence of nitrergic nerves in human uterine arteries and female genital organs has been histologically determined Yoshida et al, 1995); and the intense neurogenic relaxation mediated by NO was observed in human Nelson et al, 1995b), monkey , dog (Okamura et al, 1995), and guinea pig uterine arteries (Morris, 1993). It would be quite intriguing to clarify the physiological role of nervederived NO in the regulation of uterine circulation in women with normal pregnancies and in patients with pre-eclampsia.…”

Section: Pre-eclampsia (Pregnant Intoxication)mentioning

confidence: 99%

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The Pharmacology of Nitric Oxide in the Peripheral Nervous System of Blood Vessels

2003

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Section: E Uterine Vasculaturementioning

confidence: 90%

Section: Pre-eclampsia (Pregnant Intoxication)mentioning

confidence: 99%

The Pharmacology of Nitric Oxide in the Peripheral Nervous System of Blood Vessels

2003

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“…Being responsible for adequate perfusion of the maternal-fetal interface, the uterine vasculature undergoes dramatic changes during pregnancy to ensure continuous blood supply and nutrients to the growing uterus and fetus. Substantial remodeling (5) and sympathetic denervation (35) of the uterine arteries, enhanced uterine vasodilatation (7,49), and reduced vascular tone (44) enable the uterine vasculature to act as a low-resistance shunt to accommodate a 20-fold increase in uterine blood flow during gestation.…”

mentioning

confidence: 99%

Pregnancy reduces RhoA/Rho kinase and protein kinase C signaling pathways downstream of thromboxane receptor activation in the rat uterine artery

Goulopoulou

Hannan

Matsumoto

et al. 2012

American Journal of Physiology-Heart and Circulatory Physiology

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During pregnancy, reduced vascular responses to constrictors contribute to decreased uterine and total vascular resistance. Thromboxane A2(TxA2) is a potent vasoconstrictor that exerts its actions via diverse signaling pathways, and its biosynthesis increases in preeclampsia. In this study, we hypothesized that maternal vascular responses to TxA2will be attenuated via Rho kinase, PKC, p38 MAPK, and ERK1/2 signaling pathways. Isolated ring segments of uterine and small mesenteric arteries from late pregnant (19–21 days) and virgin rats were suspended in a myograph, and isometric force was measured. Pregnancy did not affect uterine and mesenteric artery responses to the TxA2analog U-46619 (10−9–10−5M), but transduction signals associated with these contractions were different between pregnant and nonpregnant rats. Inhibition of Rho kinase (10−6M Y-27632) reduced sensitivity to U-46619 in virgin uterine vessels but did not inhibit these contractions in pregnant uterine arteries and had no effect on mesenteric vessels. Treatment of arterial segments with a PKC inhibitor (10−6M bisindolylmaleimide I) reduced U-46619-induced contractions in virgin uterine and mesenteric arteries and in pregnant mesenteric arteries. Pregnant uterine arteries, however, were unresponsive to PKC inhibition. Inhibition of ERK1/2 (10−5M PD-98059) and p38 MAPK (10−5M SB-203580) reduced U46619-induced contractions in nonpregnant vessels and in pregnant uterine and mesenteric vessels. These data suggest that normal pregnancy does not affect uterine and mesenteric contractile responses to TxA2but reduces the contribution of Rho kinase and PKC signaling pathways to these contractions in the uterine vasculature. In contrast, the role of ERK1/2 and p38 MAPK in U-46619-induced uterine contractions remains unchanged with pregnancy. TxA2-associated transduction signals and its regulators might present potential targets for the development of new treatments for preeclampsia and other pregnancy-associated vascular diseases.

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“…We have previously reported that acetylcholine is more potent and efficacious in producing dilation of isolated uterine arteries from pregnant than from nonpregnant patients. 6,7 The acetylcholine-induced relaxation was blocked by NO synthase (NOS) inhibitors and thus is apparently mediated by NO. 6,7 Furthermore, pregnancy-induced increases in basal NO production have been found in the uterine vasculature of rats, 8,9 guinea pigs, 10,11 and sheep.…”

mentioning

confidence: 99%

“…6,7 The acetylcholine-induced relaxation was blocked by NO synthase (NOS) inhibitors and thus is apparently mediated by NO. 6,7 Furthermore, pregnancy-induced increases in basal NO production have been found in the uterine vasculature of rats, 8,9 guinea pigs, 10,11 and sheep. 3,12,13 NO is produced by NOS, of which 3 isoforms have been identified: endothelial NOS (eNOS), neuronal NOS (nNOS), and inducible NOS (iNOS).…”

mentioning

confidence: 99%

Increased Nitric Oxide Synthase Activity and Expression in the Human Uterine Artery During Pregnancy

Nelson

Steinsland

Wang

et al. 2000

Circulation Research

150

114

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Abstract-Evidence exists that NO plays a role in the vasodilation that occurs during pregnancy. The purpose of the present study was to determine whether the role of NO is associated with an increase in the activity and protein expression of NO synthase (NOS) in the human uterine artery. Uterine arteries were obtained from pregnant patients (P arteries) and nonpregnant patients (NP arteries). NOS activity was estimated with the L-[ 3 H]-arginine-to-L-[ 3 H]-citrulline conversion method and on the basis of changes in tissue levels of cGMP. Western immunoblotting and immunohistochemistry were used to assess NOS protein expression. Ca 2ϩ -dependent NOS activity was 8 times greater (PϽ0.01) in P than in NP arteries. Although most of this pregnancy-induced increase in NOS activity was Ca 2ϩ dependent (64%), a considerable portion was Ca 2ϩ independent. Expressions of endothelial NOS (eNOS) and neuronal NOS, but not inducible NOS, were demonstrated in P and NP arteries. The eNOS was located in the endothelium and stained with a qualitative order of P arteriesϾNP arteries (follicular)ϾNP arteries (luteal). The neuronal NOS was located in the adventitia of P and NP arteries. Basal NO-dependent and bradykinin-stimulated levels of cGMP were higher (PϽ0.05) in P than in NP arteries. These results indicate that an upregulation of eNOS protein expression could account for the increased NO synthesis/release in the human uterine artery during pregnancy. (Circ Res. 2000;87:406-411.)ormal pregnancy is associated with an increase in uterine blood flow and a decrease in uterine vascular resistance. [1][2][3][4] The low resistance is attributed to a loss of smooth muscle in myometrial resistance vessels (spiral arteries and terminations of radial arteries) as well as to dilation of the larger uterine arteries. 5 The dilation of the uterine arteries could be due to an increased role of endogenous vasodilators.Considerable evidence indicates that NO plays a role in pregnancy-induced uterine vasodilation. We have previously reported that acetylcholine is more potent and efficacious in producing dilation of isolated uterine arteries from pregnant than from nonpregnant patients. 6,7 The acetylcholine-induced relaxation was blocked by NO synthase (NOS) inhibitors and thus is apparently mediated by NO. 6,7 Furthermore, pregnancy-induced increases in basal NO production have been found in the uterine vasculature of rats, 8,9 guinea pigs, 10,11 and sheep. 3,12,13 NO is produced by NOS, of which 3 isoforms have been identified: endothelial NOS (eNOS), neuronal NOS (nNOS), and inducible NOS (iNOS). 14 The NOS isoforms share a common overall catalytic scheme for the oxidation of L-arginine to NO and L-citrulline but can be divided into 2 functional classes based on the dependence of Ca 2ϩ for activity. 14 The constitutive forms, eNOS and nNOS, require Ca 2ϩ for activity, but the inducible isoform, iNOS, has a Ca 2ϩ -independent activity. Ca 2ϩ -independent activity for eNOS also has been reported. [15][16][17][18] In the present study, we te...

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Pregnancy-induced alterations of neurogenic constriction and dilation of human uterine artery

Cited by 27 publications

References 0 publications

The Pharmacology of Nitric Oxide in the Peripheral Nervous System of Blood Vessels

The Pharmacology of Nitric Oxide in the Peripheral Nervous System of Blood Vessels

Pregnancy reduces RhoA/Rho kinase and protein kinase C signaling pathways downstream of thromboxane receptor activation in the rat uterine artery

Increased Nitric Oxide Synthase Activity and Expression in the Human Uterine Artery During Pregnancy

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