Effects of P2-receptor agonists on sympathetic neuroeffector transmission in the rat isolated anococcygeus muscle
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The effects of nicotinamide adenine dinucleotide phosphate (NADPH), α,β-methylene adenosine 5’-triphosphate (α,β-MeATP), l-β,γ-methylene adenosine 5’-triphosphate (l-β,γ-MeATP), 2-methylthio-adenosine 5’-triphosphate (MeSATP) and adenosine-5-O-(2’-thiodiphosphate) (ADPβS) were investigated on the contractions to electrical field stimulation in the rat anococcygeus muscle. Stimulation-induced contractions were not affected by l-β,γ-MeATP (3–100 µM) or MeSATP (3–100 µM), but were enhanced by NADPH (10–100 µM), α,β-MeATP (3–30 µM) and ADPβS (3–10 µM) in a concentration-dependent manner, and the enhancements were antagonised by the P2-receptor antagonist suramin (100 µM). The enhancement produced by α,β-MeATP (10 µM) and ADPβS (10 µM) was also antagonised by pyridoxal-phosphate-6-azophenyl-2’,4’-disulphonic acid (10 µM) and reactive blue 2 (100 µM). The enhancement produced by α,β-MeATP (10 µM) was not altered by NG-nitro-l-arginine methyl ester (100 µM), desipramine (1 µM) or idazoxan (0.1 µM) excluding, respectively, the possible involvement of nitric oxide, neuronal amine uptake or α2-autoinhibition of noradrenergic transmission. Contractions elicited by low (0.1 and 0.3 µM) but not by higher (1 and 3 µM) concentrations of exogenously applied noradrenaline were enhanced by α,β-MeATP (10 µM). Neither the resting nor the stimulation-induced effluxes of radioactivity from [3H]-noradrenaline-labelled anococcygeus muscles were affected by α,β-MeATP (10–100 µM). The findings suggest that P2-receptors subserve the enhancing actions of NADPH, α,β-MeATP and ADPβS on sympathetic neuroeffector transmission; however, the subtype of P2-receptor involved and its location remain unclear.
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