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Effects of polychlorinated biphenyl 19 (2,2',6-trichlorobiphenyl) on contraction, Ca2+ transient, and Ca2+ current of cardiac myocytes.

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dc.contributor.authorChoi, Se-Young-
dc.contributor.authorJo, Su-Hyun-
dc.contributor.authorKim, Kyong-Tai-
dc.contributor.authorLee, Chin-O-
dc.date.accessioned2010-02-01T06:02:10Z-
dc.date.available2010-02-01T06:02:10Z-
dc.date.issued2001-07-
dc.identifier.citationJournal of Cardiovascular Pharmacology 2001;38:11-20.en
dc.identifier.issn0160-2446-
dc.identifier.urihttps://hdl.handle.net/10371/47239-
dc.description.abstractPolychlorinated biphenyls (PCBs) have been known as serious
environmental pollutants, causing developmental delays, motor dysfunction,
and decrease in brain dopamine level in humans and animals. We have investigated
the effects of a PCB congener, 2,2 ,6-trichlorobiphenyl (PCB 19)
on contractile force, Ca2+ transient, and L-type Ca2+ current (ICa,L) in guinea
pig ventricular myocytes stimulated at a rate of 0.25–0.33 Hz. PCB 19 decreased
contractile force in a concentration-dependent manner. During the
negative inotropic response, the action potential duration at 20% (APD20),
90% of repolarization (APD90), and the action potential amplitude (APA)
were decreased concentration dependently: 30 M PCB 19 reduced APD20,
APD90, and APA by 36.7 ± 3.5%, 22.6 ± 3.9%, and 2.4 ± 0.6%, respectively
(n 11, p < 0.01). PCB 19 30 M decreased the Ca2+ transient and the ICa,L
by 46.8 ± 1.8% (n 9, p < 0.01) and 47.1 ± 3.1% (n 9, p < 0.01),
respectively. The results suggest that PCB 19 decreased the Ca2+ transient
through inhibition of L-type Ca2+ channels and that the decreased Ca2+ transient
consequently caused a negative inotropic effect in cardiac myocytes.
en
dc.language.isoenen
dc.publisherRaven Pressen
dc.subjectPolychlorinated biphenylen
dc.subjectContractile forceen
dc.subjectIntracellular Ca2+concentrationen
dc.subjectL-type Ca2+ currenten
dc.subjectHeart cellsen
dc.titleEffects of polychlorinated biphenyl 19 (2,2',6-trichlorobiphenyl) on contraction, Ca2+ transient, and Ca2+ current of cardiac myocytes.en
dc.typeArticleen
dc.contributor.AlternativeAuthor최세영-
dc.contributor.AlternativeAuthor조수현-
dc.contributor.AlternativeAuthor김경태-
dc.contributor.AlternativeAuthor이진오-
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