Abstract
In field-stimulated rat vas deferens, clonidine (10(-9)-10(-7) M) and alpha-methylnoradrenaline (10(-7)-3 x 10(-5) M) concentration-dependently inhibited twitch response to electrical field stimulation. The inhibitory effects of clonidine and alpha-methylnoradrenaline were similarly reduced by phenoxybenzamine (10(-6) M). However, idazoxan (3 x 10(-7) M) antagonized clonidine but not alpha-methylnoradrenaline-induced responses. The inhibitory effect of alpha-methylnoradrenaline was also not antagonized by phentolamine (3 x 10(-7) M), SK&F 104856 (2-vinyl-7-chloro-3,4,5,6-tetrahydro-4-methylthienol[4,3,2 ef][3]benzazepine) 3 x 10(-6) M) or yohimbine 3 x 10(-7) M). These antagonists however, attenuated the twitch-inhibiting effect of clonidine. The -logKB values were 8.02 +/- 0.05, 6.91 +/- 0.10, and 7.58 +/- 0.07 for phentolamine, SK&F 104856 and yohimbine respectively. In-vivo treatment of rats with N-ethoxycarbonyl-2-ethoxy-1,2-dihydroquinoline (6 mg kg-1), to inactivate prejunctional alpha 2-adrenoceptors, attenuated clonidine, but not alpha-methylnoradrenaline-induced responses. It was concluded that adrenoceptors are not involved in the prejunctional inhibitory effects of alpha-methylnoradrenaline in the rat vas deferens.
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