文摘
The adenosine-receptor modulation of noradrenaline release was compared in prostatic and epididymal portions of rat vas deferens. In both portions, tritium overflow elicited by electrical stimulation (100 pulses/8 Hz) was reduced by the adenosine A1 receptor agonist, N6-cyclopentyladenosine, and enhanced by the nonselective receptor agonist, 5′-N-ethylcarboxamidoadenosine, in the presence of the adenosine A1 receptor antagonist, 1,3-dipropyl-8-cyclopentyl-1,3-dipropylxanthine (DPCPX; 20 and 100 nM). The adenosine A2A receptor agonist, 2-p-(2-carboxyethyl)phenethyl-amino-5′-N-ethylcarboxamidoadenosine, increased tritium overflow, but only in the epididymal portion. The enhancement caused by NECA was prevented by the adenosine A2A receptor antagonist, 4-(2-[7-amino-2-(2-furyl)[1,2,4]triazolo-[2,3-a][1,3,5]triazin-5-ylamino]ethyl)phenol (ZM 241385; 20 nM), in the epididymal and by the adenosine A2B receptor antagonist, alloxazine (1 56;M), in the prostatic portion. Inhibition of adenosine uptake enhanced tritium overflow in both portions, an effect blocked by ZM 241385 in the epididymal and by alloxazine in the prostatic portion. The results indicate that adenosine exerts an adenosine A1 receptor-mediated inhibition, in both portions, and facilitation mediated by adenosine A2A receptors in the epididymal and by A2B receptors in the prostatic portion.