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Abstract Although adenosine is an important mediator of ischemic preconditioning (IPC), its relative contribution to IPC remains unknown. Because adenosine is formed through the hydrolysis of ATP, the present study investigated the role of ATP and adenosine in IPC. Isolated and buffer-perfused rat hearts underwent IPC by three cycles of 5-min ischemia and 5-min reperfusion before 25 min of global ischemia. The rate-pressure product (RPP) 30 min after reperfusion was taken as an endpoint of functional protection. Interstitial fluid (ISF) adenine nucleotides and adenosine were measured by cardiac microdialysis techniques. Inhibition of IPC-induced recovery of RPP was partial by the adenosine receptor antagonist 8-( p -sulfophenyl)theophylline (SPT; 100 μM) or by the structurally distinct P2Y purinoceptor antagonists suramin (300 μM) or reactive blue (RB; 10 μM) but was additive when SPT was given with suramin or RB. The P2X antagonist pyridoxal-phosphate-6-azophenyl-2′,4′-disulfonic acid tetrasodium (50 μM) had no effect on functional protection. The improved functional recovery was not significantly affected by an ecto-5′-nucleotidase inhibitor, α,β-methylene adenosine diphosphate (AMP-CP; 100 μM), alone but was inhibited by AMP-CP plus SPT, suramin, or RB. ISF ATP and adenosine increased temporarily by 10-fold during IPC. AMP-CP augmented the increase in ISF ATP associated with the decrease in ISF adenosine. There was a reciprocal correlation between the ISF concentration of ATP and adenosine in preconditioned hearts. In addition, there was a significant correlation between ISF adenosine and ATP and the inhibitory potency of SPT and suramin or RB against functional protection conferred by IPC. These results suggest that extracellular ATP and adenosine play a complementary role in IPC through P2Y purinoceptors and adenosine receptors, respectively. cardiac microdialysis Footnotes Present address of K. Lu: Department of Cardiothoracic Surgery, Capital University of Medical Science, Beijing Friendship Hospital, 95 Yongan Rd., Beijing, 100050 China. Address for reprint requests and other correspondence: H. Otani, Dept. of Thoracic and Cardiovascular Surgery, Kansai Medical Univ., 10-15 Fumizono-cho, Moriguchi City, Osaka 570-8507, Japan (E-mail: otanih@takii.kmu.ac.jp ). The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked “ advertisement ” in accordance with 18 U.S.C. Section 1734 solely to indicate this fact. First published January 17, 2002;10.1152/ajpheart.00760.2001 Copyright © 2002 the American Physiological Society
AJP - Heart and Circulatory Physiology – The American Physiological Society
Published: May 1, 2002
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