REPERFUSION FOLLOWING MYOCARDIAL-ISCHEMIA ENHANCES INOSITOL PHOSPHATERELEASE IN THE ISOLATED-PERFUSED RAT-HEART

Citation
Ke. Anderson et al., REPERFUSION FOLLOWING MYOCARDIAL-ISCHEMIA ENHANCES INOSITOL PHOSPHATERELEASE IN THE ISOLATED-PERFUSED RAT-HEART, Clinical and experimental pharmacology and physiology, 21(2), 1994, pp. 141-144
Citations number
11
Categorie Soggetti
Pharmacology & Pharmacy",Physiology
ISSN journal
03051870
Volume
21
Issue
2
Year of publication
1994
Pages
141 - 144
Database
ISI
SICI code
0305-1870(1994)21:2<141:RFMEIP>2.0.ZU;2-4
Abstract
1. Global myocardial ischaemia (MI) for periods greater than 5 min cau sed an inhibition of phosphatidylinositol specific phospholipase C (Pt dIns-PLC) activity. 2. Two min reperfusion following a 20 min MI perio d, a time point associated with reperfusion-induced arrhythmias, resul ted in an activation of PtdIns-PLC activity, dependent on endogenous n oradrenaline and mediated via alpha(1)-adrenoceptors. 3. This 2 min re perfusion response, in contrast to healthy myocardium, resulted in: (i ) enhanced PtdIns-PLC activity; (ii) increased sensitivity to endogeno us noradrenaline; (iii) rapid increases in inositol(l,4,5) trisphospha te (Ins(1,4,5)P-3); and (iv) PLC hydrolysis primarily of PtdIns(4,5)Pz , such that the majority of InsP isomers derive from Ins(1,4,5)P-3. 4. Together, these data suggest a functional role for Ins(1,4,5)P-3 unde r post-ischaemic reperfusion conditions, and provide a possible link b etween alpha(1)-adrenoceptor stimulation of the PtdIns turnover pathwa y and reperfusion injury.