Guanethidine-induced adrenergic-neuron blockade in rabbit vas deferens is dependent on its continued transport into adrenergic neurons via the noradrenaline transporter.
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Should not change clinical guanethidine use; extends mechanistic insight in animal models but leaves human relevance open.
The effect of neuronal-uptake inhibitors on the guanethidine-induced inhibition of responses of rabbit vas deferens to transmural stimulation was investigated. The twitch and sustained responses were inhibited by about 70% by 1.2 X 10(-5) M guanethidine. Prior or subsequent exposure to the noradrenaline-uptake inhibitors, 3.3 X 10(-5) M cocaine, 10(-5)M nisoxetine, and 10(-7)M desipramine prevented or reversed these effects of guanethidine. The depressant effects of guanethidine were not modified by the serotonin-uptake inhibitor, 10(-6)M fluoxetine. The uptake of 5 X 10(-8)M (-)-[3H]noradrenaline by rabbit vas deferens was significantly reduced by guanethidine, cocaine, nisoxetine, and desipramine, but not by fluoxetine. It was concluded that guanethidine inhibited both the twitch and sustained responses of the vas by producing adrenergic-neuron blockade and that these effects were dependent on continued transport into adrenergic neurons.
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Huston et al. (1977) studied this question.
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