Abstract
The aim of the present study was to characterize the prejunctional modulation of evoked tritium outflow in the guinea-pig vas deferens preincubated with [3H]noradrenaline. Vasa deferentia were stimulated electrically by trains of 50 pulses at 40 Hz with 4 mA. The evoked outflow of tritium was enhanced by yohimbine (1 μM, 213±38%, n=6, p<0.0001) and rauwolscine (1 μM, 201±31%, n=4, p<0.01), the α2 adrenoceptor antagonists and inhibited by clonidine (1 μM, 63±3%, n=4, p<0.05), the α2 agonist. The P2 purinoceptor antagonists suramin (300 μM, 94±9%, n=5) and pyridoxalphosphate-6-azophenyl-2',4'-disulfonic acid (PPADS, 30 μM, 100±2%, n=4) did not significantly change the tritium outflow. The tritium outflow was enhanced by BK channel antagonists iberiotoxin (100 nM, 127±9%, n=7, p<0.001) and γcharybdotoxin (100 nM, 145±22%, n=10, p<0.001), and decreased by SK channel antagonist apamin (100 nM, 88±8%, n=6, p<0.01). L-type Ca2+ channel agonist, Bay K 8644 (1 μM, n=8) and antagonists, nifedipine (40 μM, n=8), nimodipine (10 μM, n=4) and nicardipine (20 μM, n=4) did not affect on the spontaneous and evoked outflow of tritium. Nw-nitro-L-arginine (100 μM, n=6), an inhibitor of NO synthase, and sodium nitroprusside (100 μM, n=6), a NO donor had no significant effect on the evoked outflow of tritium. These results indicate that α2 adrenoceptors and BK channels play an important role in a prejunctional modulation of neuronal noradrenaline release in the guinea-pig vas deferens. [Jpn J Physiol 54 Suppl:S122 (2004)]
