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흰쥐 적혈구세포막에 Aenosine Triphosphatase에 미치는 Diphenyhydantion의 영향 : The Effects of Diphenylhydantoin on Adenosine Triphosphatase Activity in Rat Erythrocyte Membranes

DC Field Value Language
dc.contributor.author이정윤-
dc.date.accessioned2009-08-31T15:37:22Z-
dc.date.available2009-08-31T15:37:22Z-
dc.date.issued1970-12-01-
dc.identifier.citationSeoul J Med, Vol.11 No.4, pp. 11-18-
dc.identifier.issn0582-6802-
dc.identifier.urihttps://hdl.handle.net/10371/8231-
dc.description.abstractThe effects of diphenylhydantoin on ATPase activity
in rat erythrocyte membranes were studied and also
influence of K+ on ATPase activity was studied.
The ATPase activity of rat erythrocyte membranes
has been shown to consist of two components.
The first component requires the Mg"! in the absence
of Naror K+ (MgH -A'I'Pase) and is not inhibited by
ouabain and stimulated by diphenylhydantoin.
The second component requires the presence of MgH
and also Nar or K+ (Nar -K+ -A'I'Pase). It is inhibited
by ouabain and is stimulated by diphenylhydantoin in
10'.'1' Nat concentration and inhibited in high Na!
concentration.
Potassium ion reverse the Na' -Kr-A'I'Pase which
is inhibited by ouabain.
Ouabain and diphenylhydantoin show reversed effect
to Na+-K+-ATPase activity.
It suggests that the therapeutic effect of diphenylhydantoin
0:1 digitalis induced cardiac arrhythmia may
be resulted from their effect on ion transport mechanism
of ceIl membrane.
And the relevance of these findings to the action of
ouabain and diphenylhydantoin on membrane transport
mechanism is discussed.
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dc.language.isoko-
dc.publisher서울대학교 의과대학-
dc.title흰쥐 적혈구세포막에 Aenosine Triphosphatase에 미치는 Diphenyhydantion의 영향-
dc.title.alternativeThe Effects of Diphenylhydantoin on Adenosine Triphosphatase Activity in Rat Erythrocyte Membranes-
dc.typeSNU Journal-
dc.contributor.AlternativeAuthorLee, Jung Yoon-
dc.citation.journaltitle서울 의대 잡지-
dc.citation.journaltitle서울 의대 학술지-
dc.citation.journaltitleSeoul Journal of Medicine-
dc.citation.endpage18-
dc.citation.number4-
dc.citation.pages11-18-
dc.citation.startpage11-
dc.citation.volume11-
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