Abstract

The inhibitory effect of adenosine on the electrically evoked contractions in the rat prostatic vas deferens was markedly dependent on the calcium concentration in the medium, with adenosine being 20 times more potent at lower calcium levels (1.26 mM vs 3.6 mM). Similar calcium dependence of adenosine inhibition was observed in the presence of a potent nucleoside uptake inhibitor, nitrobenzylthioguanosine (NBTGR), suggesting that this calcium dependence of adenosine inhibition was not secondary to an alteration in adenosine uptake. Furthermore, Bay K8644 (methyl-1,4-dihydro-2,6-dimethyl-3-nitro-4-(2-trifluoromethylphenyl)pyridine-5-carboxylate), a dihydropyridine ‘calcium entry activator’, reduced the potency of adenosine in inhibiting the electrically evoked contractions in a calcium-dependent manner. These results support the notion that adenosine might exert its inhibition on neurotransmission in the prostatic rat vas deferens by decreasing transmembrane calcium currents into the nerve terminals and/or the smooth muscles.

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