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

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Grover, G.J. et al.

The cardioprotective effects of R 75231 and lidoflazine are not caused by adenosine A1 receptor activation.

The goal of this study was to determine the cardioprotective profile for the nucleoside transport inhibitor 2-(aminocarboxyl)-N-(4-amino-2,6-dichlorophenyl)-4-[5,5-bis(4- fluorophenyl)pentyl]-1-piperazinylacetamide trihydrochloride-2,5 hydrate (R 75231) in isolated rat hearts and whether its protective effects are caused by adenosine A1 activation. R 75231 increased time to contracture during global ischemia in a concentration-dependent manner (EC25 = 2.6 microM) that was comparable to the structurally related compound lidoflazine (EC25 = 1.2 microM). R 75231 caused only modest improvements in reperfusion contractile function, whereas it profoundly reduced LDH release. The cardioprotective effects of R 75231 were accompanied by preischemic negative inotropy with modest bradycardic effects. Adenosine also increased time to contracture, although it was not very potent (EC25 > 300 microM), and this effect was accompanied by significant preischemic bradycardia without measurable negative inotropic activity. Both the preischemia bradycardia and increase in ischemic time to contracture with adenosine were abolished completely by the A1 blocker 8-cyclopentyl-1,3-dipropylxanthine. The adenosine-induced increase in time to contracture was reversed partially by glybenclamide. Neither the pre- nor postischemic effects of R 75231 were abolished by 8-cyclopentyl-1,3-dipropylxanthine or glybenclamide, except for the preischemic bradycardia. Similar results were observed for lidoflazine. Thus, the cardioprotective effects of R 75231 are not mediated by adenosine A1 receptor activation and, thus, probably are not caused by its activity as a nucleoside transport inhibitor. It may be acting as a calcium antagonist in this model.[1]

References

The cardioprotective effects of R 75231 and lidoflazine are not caused by adenosine A1 receptor activation. Grover, G.J., Sleph, P.G. J. Pharmacol. Exp. Ther. (1994) [Pubmed]

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