XANTHINE AFFECTS [CA2-STIMULATION(](I) AND CONTRACTILE RESPONSES OF VENTRICULAR CARDIOCYTES TO ELECTRICAL)

Citation
Tt. Rohn et al., XANTHINE AFFECTS [CA2-STIMULATION(](I) AND CONTRACTILE RESPONSES OF VENTRICULAR CARDIOCYTES TO ELECTRICAL), American journal of physiology. Cell physiology, 42(3), 1997, pp. 909-917
Citations number
30
Categorie Soggetti
Physiology
ISSN journal
03636143
Volume
42
Issue
3
Year of publication
1997
Pages
909 - 917
Database
ISI
SICI code
0363-6143(1997)42:3<909:XA[ACR>2.0.ZU;2-O
Abstract
Xanthine, a major purine by-product of ATP, accumulates during myocard ial ischemia. In the present study, we show that xanthine (0.5-1 mM) i mpaired the occurrence of cytosolic Ca2+ concentration ([Ca2+](i)) tra nsients, visualized in fura 2-loaded cells, and twitches of contractio n in ventricular cardiocytes in response to electrical stimulation. Th is effect of xanthine was independent of superoxide anion production. That it was a result of decreased membrane excitability was supported by the following: I)it was reversed by increasing either the amplitude of the stimulus voltage required to stimulate cardiocytes or the extr acellular concentration of NaCl; and 2) xanthine reversed the depolari zation following electrical stimulation in cardiocytes loaded. with th e voltage-sensitive dye bis-oxonol. P-2 purinergic-agonists, including ATP (10 mu M), but not P-1 purinergic agonists reproduced the effects seen with xanthine. In addition, a lack of additivity between xanthin e and ATP at maximal concentrations was observed. We conclude that xan thine, through activation of a Pg purinoceptor, may contribute to myoc ardial arrhythmia occurring during ischemia-reperfusion injury.