期刊
EXPERIMENTAL BIOLOGY AND MEDICINE
卷 237, 期 8, 页码 966-972出版社
ROYAL SOC MEDICINE PRESS LTD
DOI: 10.1258/ebm.2012.012006
关键词
perfused heart; purinergic P2Y receptors; coronary circulation; K-ATP potassium channels; nitric oxide; Langendorff preparation
资金
- Fondo de Investigaciones Sanitarias [PS09/00394]
- Fundacion Mutua Madrilena [AP57242009]
Diadenosine triphosphate (Ap3A) is a vasoactive mediator stored in platelet granules that may be released during coronary ischemia-reperfusion. To study its coronary effects in such circumstances, rat hearts were perfused in a Langendorff preparation and the coronary response to Ap3A (10(-7)-10(-5) mol/L) was recorded. Both at basal coronary resting tone and after precontraction with 11-dideoxy-1a,9a-epoxymethanoprostaglandin F-2 alpha (U46619), Ap3A produced concentration-dependent vasodilation in the heart, which was attenuated following ischemia-reperfusion. Ap3A-induced relaxation was also attenuated in control conditions and after ischemia-reperfusion by the purinergic P2Y antagonist reactive blue 2 (2 x 10(-6) mol/L), the P2Y(1) antagonist MRS 2179 (10(-5) mol/L), the nitric oxide synthesis inhibitor N-omega-nitro-L-arginine methyl ester (L-NAME; 10(-4) mol/L) and the ATP-dependent potassium channel blocker glibenclamide (10(-5) mol/L). These results suggest that Ap3A induces coronary vasodilation, an effect attenuated by ischemia-reperfusion due to the functional impairment of purinergic P2Y receptors and K-ATP channels, and/or reduced nitric oxide release. This impairment of vasodilation may contribute to the coronary dysregulation that occurs during ischemia-reperfusion.
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