Effect of the vascular endothelium on noradrenaline‐induced contractions in non‐pregnant and pregnant guinea‐pig uterine arteries

Jovanović, Aleksandar; Grbović, Leposava; Jovanović, Sofija

doi:10.1111/j.1476-5381.1995.tb13276.x

Cited by 23 publications

(4 citation statements)

References 44 publications

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“…This may be due to the high intrinsic activity of acetylcholine that may result in difficulties to block NO‐synthase activity in the presence of such a strong agonist (Jovanović et al., 1994c). The release of a, yet unidentified, endothelium‐dependent relaxant factor may also be alternatively possible (Jovanović et al., 1995b).…”

Section: Discussionmentioning

confidence: 99%

Endothelium‐dependent Relaxation of Canine Uterine Artery in Response to Acetylcholine: the Possible Involvement of Alternative Pathways

Pesic

Grbović

Jovanović

et al. 2003

Journal of Veterinary Medicine Series A

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The effect of acetylcholine on the isolated, pre-contracted, uterine artery of non-pregnant dog was investigated. Acetylcholine-induced concentration-dependent relaxation of isolated canine uterine artery with endothelium (pEC50 = 6.48 +/-0.01, n = 37) and was without effect on arterial segments denuded of endothelium. Indomethacin, 4-aminopyridine (10-5 m) and pre-contraction with K+-rich Krebs-Ringer bicarbonate solution had no effect on acetylcholine-induced relaxation. NG-nitro-l-arginine (l-NOARG) (10-5 m) inhibited relaxation evoked by acetylcholine. Indomethacin applied with l-NOARG led to further inhibition of acetylcholine-induced relaxation. In the presence of both l-NOARG and indomethacin, 4-aminopiridine did not provoke further inhibition of acetylcholine-induced relaxation of canine uterine artery. It is concluded that the acetylcholine-induced relaxation of canine uterine artery is probably mediated by endothelial production of nitric oxide (NO). However, if NO-synthase is inhibited, acetylcholine-induced vasorelaxation may be, in part, mediated through activation of cyclooxygenase pathway.

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Section: Discussionmentioning

confidence: 99%

Endothelium‐dependent Relaxation of Canine Uterine Artery in Response to Acetylcholine: the Possible Involvement of Alternative Pathways

Pesic

Grbović

Jovanović

et al. 2003

Journal of Veterinary Medicine Series A

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“…It is possible that this small relaxation to acetylcholine may be due to high intrinsic activity of acetylcholine that may result in difficulties to block NO-synthase activity in the presence of such strong agonist [21]. Alternatively, release of an as yet unidentified endothelium-dependent relaxant factor may be also possible [22].…”

Section: Resultsmentioning

confidence: 99%

Endothelium-Dependent Relaxation in Perforating Branch of Human Internal Mammary Artery

Pešić,

Jovanović,

Grbović

et al. 2000

Cardiovascular Surgery

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The purpose of the present study was to examine the effect of acetylcholine on perforating branch of the human internal mammary artery (HIMA). Acetylcholine (10−9–10−5 M) induced concentration- and endothelium-dependent relaxation (pEC50 = 7.54 ± 0.03, maximal response was 98 ± 1.3%) of the precontracted arterial segments. Indomethacin, 4-aminopyridine (10−5 M) and precontraction with K+-rich Krebs—Ringer–bicarbonate solution had no effect on acethylcholine-induced relaxation. NG-monomethyl-L-arginine (L-NMMA) (10−5 M) inhibited relaxation evoked by acetylcholine. Indomethacin applied together with L-NMMA lead to further inhibition of acethylcholine-induced relaxation. Even in the presence of both L-NMMA and indomethacin, 4-aminopyridine had no provoked further inhibition of acetylcholine-induced relaxation of perforating branch of HIMA. It was concluded that the acethylcholine-induced relaxation of isolated perforating branch of HIMA is probably mediated via endothelial production of nitric oxide. However, when NO-synthase is inhibited, acetylcholine-induced vasorelaxation may be, in part, mediated through activation of cyclooxygenase pathway and consequent production and release of prostacyclin or some other cyclooxygenase products.

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“…The increased α 2 -mediated vasorelaxation was dependent on the endothelium and nitric oxide synthase (NOS). Several studies in isolated uterine arteries from pregnant humans and various experimental animal models [51][52][53][54][55][56][57] have demonstrated that endothelium-dependent and independent pathways play increased roles in buffering adrenergic receptor-induced vasoconstriction in pregnant versus non-pregnant groups. These enhanced vasodilatory and vasoconstriction-buffering mechanisms are mediated by increased NOS, vascular smooth muscle cell responsiveness to vasodilators, and reduced capacity of the smooth muscle layer to depolarize [54,58].…”

Section: Mechanisms To Buffer Sna-mediated Control Of Maternal Hemodynamics During Normal Pregnancymentioning

confidence: 99%

Sympathetic nervous system control of vascular function and blood pressure during pregnancy and preeclampsia

Spradley

2019

Journal of Hypertension

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: Proper vascular tone and blood pressure regulation during pregnancy are important for immediate and long-term cardiovascular health of the mother and her offspring. Preeclampsia is clinically defined as new-onset maternal hypertension accompanied by cardiovascular, renal, and/or neural abnormalities presenting in the second half of pregnancy. There is strong evidence to support that preeclampsia is mediated by attenuations in uteroplacental vascular remodeling and increases in vasoconstriction with subsequent placental ischemia/reperfusion-induced release of hypertensive substances into the maternal circulation. These include antiangiogenic and pro-inflammatory factors. There is also evidence implicating increased sympathetic nervous system activity (SNA) in this maternal disorder, but this mostly includes data correlating severity of disease with catecholamine levels and elevated muscle SNA. These measurements have not confirmed a causative role for SNA in the pathogenesis of preeclampsia. Therefore, studies are needed to provide a comprehensive understanding of SNA and its control of vascular function and blood pressure regulation during normal pregnancy in order to set the stage for exploring the mechanisms mediating the exaggerated SNA and signaling during preeclampsia. This review examines the role of SNA in control of uteroplacental vascular tone and blood pressure regulation during normal pregnancy. Furthermore, it is proposed that over-activation of the SNA contributes to altered uteroplacental vascular tone and perfusion leading to placental ischemic events and modulates the systemic vasoconstriction and hypertensive responses to soluble placenta ischemic factors. Recognizing the integrative role and importance of SNA in the pathophysiology of preeclampsia will advance our understanding of this maternal disorder.

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Effect of the vascular endothelium on noradrenaline‐induced contractions in non‐pregnant and pregnant guinea‐pig uterine arteries

Cited by 23 publications

References 44 publications

Endothelium‐dependent Relaxation of Canine Uterine Artery in Response to Acetylcholine: the Possible Involvement of Alternative Pathways

Endothelium‐dependent Relaxation of Canine Uterine Artery in Response to Acetylcholine: the Possible Involvement of Alternative Pathways

Endothelium-Dependent Relaxation in Perforating Branch of Human Internal Mammary Artery

Sympathetic nervous system control of vascular function and blood pressure during pregnancy and preeclampsia

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