Increased myocardial inositol trisphosphate levels during α1-adrenergic stimulation and reperfusion of ischaemic rat heart

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dc.contributor.authorMouton R.
dc.contributor.authorHuisamen B.
dc.contributor.authorLochner A.
dc.date.accessioned2011-05-15T15:59:43Z
dc.date.available2011-05-15T15:59:43Z
dc.date.issued1991
dc.description.abstractAlthough stimulated [3H] inositol phosphate turnover has been demonstrated in isolated, perfused [3H] inositol prelabelled rat hearts, there is still no information regarding Ins(1,4,5)P3 levels in intact cardiac muscle. Using a D-myo-Ins(1,4,5)P3 assay system, Ins(1,4,5)P3 levels were determined in isolated perfused rats hearts during ischaemia, reperfusion and α1-adrenergic stimulation via noradrenaline (3 x 10-5M). Control hearts contained ± 674 pmols Ins(1,4,5)P3/g dry heart weight. Myocardial Ins(1,4,5) P3 levels were significantly decreased (± 389 pmols/g dry heart weight) after exposure to 20 mins of normothermic ischaemic cardiac arrest(NICA). Reperfusion produced a marked increase in Ins(1,4,5,)P3 levels(± 1 115pmols/g dry heart weight) after only 30 s. Noradrenaline caused a 3-4 fold increase in tissue Ins(1,4,5)P3 levels within 30 s. After 20 mins stimulation with noradrenaline, the Ins(1,4,5)P3 levels were still significantly elevated. The rise in tissue Ins(1,4,5)P3 levels during reperfusion as well as during noradrenaline administration was counteracted by neomycin (0.5 x 10-3 M), an inhibitor of phosphoinositidase specific phospholipase C. In both events neomycin restored the Ins( 1,4,5)P3 levels to control values. For correlation of tissue Ins (1,4,5)P3 levels with mechanical events, noradrenaline (3 x 10-5 M), in the presence of 10 mM LiCl, 10-7 M propanolol and 10-7 M atropine, was administered to isolated perfused rat hearts and the mechanical performance recorded over a period of 20 mins. Noradrenaline caused a significant increase in peak systolic pressure and work performance which was maintained for at least 10 mins, suggesting that the positive inotropic effects of noradrenaline may be provoked by Ins(l,4,5)P3. Furthermore, the finding that 20 min NICA followed by 30 s reperfusion causes an immediate significant increase in Ins(1,4,5)P3 content suggests a role for the phosphatidylinositol pathway in the intracellular Ca2+ overloading, characteristic of ischaemia-reperfusion.
dc.description.versionArticle
dc.identifier.citationJournal of Molecular and Cellular Cardiology
dc.identifier.citation23
dc.identifier.citation7
dc.identifier.issn222828
dc.identifier.other10.1016/0022-2828(91)90217-A
dc.identifier.urihttp://hdl.handle.net/10019.1/11331
dc.subjectalpha 1 adrenergic receptor
dc.subjectatropine
dc.subjectinositol 1,4,5 trisphosphate
dc.subjectlithium chloride
dc.subjectneomycin
dc.subjectnoradrenalin
dc.subjectphosphatidylinositide
dc.subjectphosphatidylinositol
dc.subjectphospholipase c
dc.subjectpropranolol
dc.subjectalpha adrenergic stimulation
dc.subjectanimal tissue
dc.subjectarticle
dc.subjectassay
dc.subjectcalcium cell level
dc.subjectheart muscle
dc.subjectheart muscle ischemia
dc.subjectheart muscle reperfusion
dc.subjectheart weight
dc.subjectinotropism
dc.subjectmale
dc.subjectnonhuman
dc.subjectphosphoinositide metabolism
dc.subjectpriority journal
dc.subjectrat
dc.subjectsystolic blood pressure
dc.subjecttissue level
dc.subjectAnimalia
dc.subjectNica
dc.titleIncreased myocardial inositol trisphosphate levels during α1-adrenergic stimulation and reperfusion of ischaemic rat heart
dc.typeArticle
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