Analysis of calcium responses mediated by the A3 adenosine receptor in cultured newborn rat cardiac myocytes.
作者： Vladimir Shneyvays , Tova Zinman , Asher Shainberg
DOI: 10.1016/J.CECA.2004.03.004
关键词:
摘要: Abstract Intracellular calcium signaling cascade induced by adenosine A 3 receptor activation was studied in this work. It found that (and not 1 or 2A receptors activation) leads to an increase cytosolic and its further extrusion. selective agonist Cl-IB-MECA (2-chloro- N 6 -(3-iodobenzyl)adenosine-5′- -methyluronamide) cytoplasmic a dose-dependent manner, independent on extracellular calcium. The Ca 2+ signal newborn cardiomyocytes, activation, is dependent pertussis toxin-sensitive G-protein. action of inhibited inhibitor phospholipase C (PLC), antagonists inositol 1,4,5-trisphosphate (IP ) receptor. In contrast, inhibition ryanodine prevented elevation agonist. shown extrusion the elevated achieved via sarcoplasmic reticulum (SR) -reuptake sarcolemmal Na + /Ca exchanger (NCX). SR -uptake NCX efflux were sufficient only for compensation release from after but also effective prevention extensive intracellular may provide mechanism against cellular overload. cells with [Ca ] i (due o ), decreased toward diastolic control level, whereas ineffective. protective effect abolished presence antagonist MRS1523.
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