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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

Evaluation of N-0861, (+-)-N6-endonorbornan-2-yl-9-methyladenine, as an A1 subtype-selective adenosine receptor antagonist in the guinea pig isolated heart.

Activation of cardiac A1 adenosine receptors slows atrioventricular conduction and attenuates the effects of catecholamines, whereas activation of A2 adenosine receptors causes coronary dilation. This study investigates the antagonism of the action of adenosine on A1 and A2 adenosine receptor subtypes by (+-)-N6-endonorbornan-2-yl-9-methyladenine (N-0861) in guinea pig isolated perfused hearts. Stimulus to His bundle interval, coronary perfusion pressure and left ventricular pressure were measured. In normoxic hearts, N-0861 competitively and reversibly antagonized stimulus to His bundle interval prolongation induced by adenosine (1-30 microM) but not that caused by carbachol (0.09 microM), verapamil (1 microM), MgCl2 (6.5 mM) or hypothermia. N-0861 (up to 100 microM) did not attenuate the decrease in coronary perfusion pressure caused by adenosine. N-0861 significantly attenuated the antagonism by adenosine of an isoproterenol-mediated elevation of left ventricular pressure. N-0861 significantly reduced stimulus to His bundle prolongation induced by either hypoxia or reduced perfusion ("ischemia") but did not attenuate the hypoxia-induced decrease in coronary perfusion pressure. Receptor binding studies indicated that N-0861 competitively displaced the binding of 8-cyclopentyl-1,3-[3H]dipropylxanthine to crude guinea pig and human atrial membranes (Ki values of 0.62 and 0.7 microM, respectively) but did not displace the binding of S-(p-nitro[3H]benzyl)-6-thioinosine. The results indicate that in the heart N-0861 is a reversible, specific and selective antagonist of adenosine at the A1 receptor subtype.[1]


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