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Heterogeneity of the SR-dependent Inward Na+-Ca2+ Exchange Current in the Heavily Ca2+ - Buffered rat Ventricular Myocytes

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dc.contributor.author윤경봉-
dc.date.accessioned2015-07-14T17:25:31Z-
dc.date.available2015-07-14T17:25:31Z-
dc.date.issued2004-
dc.identifier.issn1226-4512-
dc.identifier.urihttps://ir.ymlib.yonsei.ac.kr/handle/22282913/112855-
dc.description.abstractVoltage-sensitive release mechanism was pharmacologically dissected from the Ca2+-induced Ca2+ release in the SR Ca2+ release in the rat ventricular myocytes patch-clamped in a whole-cell mode. SR Ca2+ release process was monitored by using forward-mode Na+-Ca2+ exchange after restriction of the interactions between Ca2+ from SR and Na+-Ca2+ exchange within micro-domains with heavy cytosolic Ca2+ buffering with 10 mM BAPTA. During stimulation every 10 s with a pulse roughly mimicking action potential, the initial outward current gradually turned into a huge inward current of -12.9+/-0.5 pA/pF. From the inward current, two different inward INCXs were identified. One was 10 muM ryanodine-sensitive, constituting 14.2+/-2.3%. It was completely blocked by CdCl2 (0.1 mM and 0.5 mM) and by Na+-depletion. The other was identified by 5 mM NiCl2 after suppression of ICaL and ryanodine receptor, constituting 14.8+/-1.6%. This latter was blocked by either 10 mM caffeine-induced SR Ca2+-depletion or 1 mM tetracaine. IV-relationships illustrated that the latter was activated until the peak in 30~35 mV lower voltages than the former. Overall, it was concluded that the SR Ca2+ release process in the rat ventricular myocytes is mediated by the voltage-sensitive release mechanism in addition to the Ca2+-induced-Ca2+ release.-
dc.description.statementOfResponsibilityopen-
dc.format.extent101~110-
dc.relation.isPartOfKOREAN JOURNAL OF PHYSIOLOGY & PHARMACOLOGY-
dc.rightsCC BY-NC-ND 2.0 KR-
dc.rights.urihttps://creativecommons.org/licenses/by-nc-nd/2.0/kr/-
dc.titleHeterogeneity of the SR-dependent Inward Na+-Ca2+ Exchange Current in the Heavily Ca2+ - Buffered rat Ventricular Myocytes-
dc.typeArticle-
dc.contributor.collegeCollege of Medicine (의과대학)-
dc.contributor.departmentDept. of Anesthesiology (마취통증의학)-
dc.contributor.googleauthorKyung-Bong Yoon-
dc.contributor.googleauthorSung-Wan Ahn-
dc.contributor.googleauthorChang Mann Ko-
dc.admin.authorfalse-
dc.admin.mappingfalse-
dc.contributor.localIdA02539-
dc.relation.journalcodeJ02104-
dc.identifier.eissn2093-3827-
dc.subject.keywordVoltage-sensitive release mechanism-
dc.subject.keywordCa2+-induced Ca2+ release-
dc.subject.keywordHeavy Ca2+-buffering-
dc.subject.keywordNa+-Ca2+ exchange-
dc.subject.keywordSR-
dc.subject.keywordRat heart-
dc.contributor.alternativeNameYoon, Kyoung Bong-
dc.contributor.affiliatedAuthorYoon, Kyoung Bong-
dc.rights.accessRightsfree-
dc.citation.volume8-
dc.citation.number2-
dc.citation.startPage101-
dc.citation.endPage110-
dc.identifier.bibliographicCitationKOREAN JOURNAL OF PHYSIOLOGY & PHARMACOLOGY, Vol.8(2) : 101-110, 2004-
dc.identifier.rimsid36756-
dc.type.rimsART-
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Anesthesiology and Pain Medicine (마취통증의학교실) > 1. Journal Papers

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