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Article: Role of extracellular calcium and calcium channels in the response of human placental venous smooth muscle to endothelin-1

TitleRole of extracellular calcium and calcium channels in the response of human placental venous smooth muscle to endothelin-1
Authors
Issue Date1993
PublisherMosby, Inc. The Journal's web site is located at http://www.elsevier.com/locate/ajog
Citation
American Journal Of Obstetrics And Gynecology, 1993, v. 169 n. 6, p. 1427-1430 How to Cite?
AbstractObjective: Our purpose was to evaluate the role of calcium and calcium channels in endothelin-1-induced contraction of the smooth muscle of human placental veins. Study design: Placentas were collected after vaginal delivery at term. After their removal from the chorionic plate, placental veins were divided into rings that were suspended in organ chambers and stretched to optimal tension. In the first part of the study, vessels from six women were initially suspended in calcium-poor modified Krebs-Ringer solution. They were then treated with either EGTA [ethylene glycol-bis(β-aminoethyl ether)N,N,N',N'-tetraacetic acid; calcium chelator, 0.5 mmol/L] or calcium chloride 2.5 mmol/L (control). Endothelin-1 was then added cumulatively (10-10 to 10-7 mol/L), and the resulting changes in isometric tensions were recorded. In the second part of the study vessels from six other women were treated with either (1) normal modified Krebs-Ringers solution (control), (2) calcium-poor modified Krebs-Ringers solution, or (3) nicardipine (dihydropyridine calcium channel inhibitor, 10-7 mol/L) in separate organ chambers. Endothelin-1 was then added cumulatively. Results: Endothelin-1 produced concentration-dependent contractions in placental veins, with maximal tension reached at 10-7 mol/L. Substitution of calcium-poor for standard Krebs-Ringers solution in the organ chamber abolished contractions to low endothelin-1 concentrations (≤ 10-9 mol/L, p < 0.001) but did not affect the contractile response to higher concentrations. EGTA abolished contractions to all concentrations tested (p < 0.02). Nicardipine significantly, but incompletely, inhibited the contractile responses to all endothelin-1 concentrations tested (p < 0.05). Conclusions: Endothelin-1 induces contraction of the smooth muscle of human placental veins, which requires the influx of extracellular calcium. Dihydropyridine-sensitive calcium channels represent a major route of entry, but other pathways participate. The fetal effects of nifedipine and other calcium-channel blockers deserve specific evaluation in intrauterine growth retardation and other pregnancies complicated by elevated fetal levels of endothelin-1.
Persistent Identifierhttp://hdl.handle.net/10722/171082
ISSN
2015 Impact Factor: 4.681
2015 SCImago Journal Rankings: 2.255
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorLe, SQen_US
dc.contributor.authorWasserstrum, Nen_US
dc.contributor.authorMombouli, JVen_US
dc.contributor.authorVanhoutte, PMen_US
dc.date.accessioned2012-10-30T06:12:07Z-
dc.date.available2012-10-30T06:12:07Z-
dc.date.issued1993en_US
dc.identifier.citationAmerican Journal Of Obstetrics And Gynecology, 1993, v. 169 n. 6, p. 1427-1430en_US
dc.identifier.issn0002-9378en_US
dc.identifier.urihttp://hdl.handle.net/10722/171082-
dc.description.abstractObjective: Our purpose was to evaluate the role of calcium and calcium channels in endothelin-1-induced contraction of the smooth muscle of human placental veins. Study design: Placentas were collected after vaginal delivery at term. After their removal from the chorionic plate, placental veins were divided into rings that were suspended in organ chambers and stretched to optimal tension. In the first part of the study, vessels from six women were initially suspended in calcium-poor modified Krebs-Ringer solution. They were then treated with either EGTA [ethylene glycol-bis(β-aminoethyl ether)N,N,N',N'-tetraacetic acid; calcium chelator, 0.5 mmol/L] or calcium chloride 2.5 mmol/L (control). Endothelin-1 was then added cumulatively (10-10 to 10-7 mol/L), and the resulting changes in isometric tensions were recorded. In the second part of the study vessels from six other women were treated with either (1) normal modified Krebs-Ringers solution (control), (2) calcium-poor modified Krebs-Ringers solution, or (3) nicardipine (dihydropyridine calcium channel inhibitor, 10-7 mol/L) in separate organ chambers. Endothelin-1 was then added cumulatively. Results: Endothelin-1 produced concentration-dependent contractions in placental veins, with maximal tension reached at 10-7 mol/L. Substitution of calcium-poor for standard Krebs-Ringers solution in the organ chamber abolished contractions to low endothelin-1 concentrations (≤ 10-9 mol/L, p < 0.001) but did not affect the contractile response to higher concentrations. EGTA abolished contractions to all concentrations tested (p < 0.02). Nicardipine significantly, but incompletely, inhibited the contractile responses to all endothelin-1 concentrations tested (p < 0.05). Conclusions: Endothelin-1 induces contraction of the smooth muscle of human placental veins, which requires the influx of extracellular calcium. Dihydropyridine-sensitive calcium channels represent a major route of entry, but other pathways participate. The fetal effects of nifedipine and other calcium-channel blockers deserve specific evaluation in intrauterine growth retardation and other pregnancies complicated by elevated fetal levels of endothelin-1.en_US
dc.languageengen_US
dc.publisherMosby, Inc. The Journal's web site is located at http://www.elsevier.com/locate/ajogen_US
dc.relation.ispartofAmerican Journal of Obstetrics and Gynecologyen_US
dc.subject.meshAdulten_US
dc.subject.meshCalcium - Physiologyen_US
dc.subject.meshCalcium Channels - Drug Effects - Physiologyen_US
dc.subject.meshEndothelins - Physiologyen_US
dc.subject.meshExtracellular Spaceen_US
dc.subject.meshFemaleen_US
dc.subject.meshHumansen_US
dc.subject.meshMuscle Contraction - Physiologyen_US
dc.subject.meshMuscle, Smooth, Vascular - Physiologyen_US
dc.subject.meshNicardipine - Pharmacologyen_US
dc.subject.meshPlacenta - Blood Supplyen_US
dc.subject.meshPregnancyen_US
dc.titleRole of extracellular calcium and calcium channels in the response of human placental venous smooth muscle to endothelin-1en_US
dc.typeArticleen_US
dc.identifier.emailVanhoutte, PM:vanhoutt@hku.hken_US
dc.identifier.authorityVanhoutte, PM=rp00238en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1016/0002-9378(93)90413-D-
dc.identifier.pmid8267041-
dc.identifier.scopuseid_2-s2.0-0027144079en_US
dc.identifier.volume169en_US
dc.identifier.issue6en_US
dc.identifier.spage1427en_US
dc.identifier.epage1430en_US
dc.identifier.isiWOS:A1993MN38300009-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridLe, SQ=7006184502en_US
dc.identifier.scopusauthoridWasserstrum, N=7004673923en_US
dc.identifier.scopusauthoridMombouli, JV=7004285772en_US
dc.identifier.scopusauthoridVanhoutte, PM=7202304247en_US

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