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Naunyn Schmiedebergs Arch Pharmacol. 1984 Dec;328(2):148-53.

Amphetamine-clonidine interaction on neurotransmission in the vas deferens of the rat.


The interaction between amphetamine and clonidine on neurotransmission in the rat vas deferens was studied. In the whole vas deferens, clonidine 0.037 mumol/l displaced to the right the frequency-response curve evoked by either hypogastric or field stimulation. The frequency of stimulation that produced 50% of the maximal response (EF 50) was: control 4.0 Hz, clonidine 18.3 Hz (P less than 0.001 n = 4), for hypogastric nerve stimulation; and 2.1 Hz in controls and 17.1 Hz in clonidine-treated preparations, for field stimulation (P less than 0.001 n = 5). Preincubation with 5.4 mumol/l amphetamine antagonized the effect of clonidine (EF 50 amphetamine alone 6.2 Hz, amphetamine + clonidine 7.3 Hz; P greater than 0.5). After 12 min of incubation with clonidine 0.037 mumol/l the responses to 6.4 Hz (3 s, 0.5 ms) were decreased by 77 +/- 2.2%. Both yohimbine and amphetamine, in a concentration-dependent manner, attenuated the inhibition. Washout of clonidine produced a slow recovery of the responses. Inhibition of the motor response to nerve stimulation (6.4 Hz, 3 s) by 30 mumol/l 2',3'-cAMP was increased by 10 mumol/l dipyridamole and impaired by 100 mumol/l theophylline. Amphetamine, in a concentration that markedly reduced clonidine inhibition of neurotransmission failed to antagonize 2',3'-cAMP. In the bisected vas deferens clonidine inhibited the peak motor response to short trains of field stimuli in the prostatic portion ("non-adrenergic") and the sustained response in the epididymal portion ("adrenergic"). Yohimbine potentiated both types of responses and fully prevented the effect of clonidine. In the prostatic portion amphetamine slightly inhibited the peak motor response and attenuated the inhibitory effect of clonidine in both portions of the vas.(ABSTRACT TRUNCATED AT 250 WORDS).

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