Effects of in vitro, acute and chronic treatment with fluoxetine on the sympathetic neurotransmission of rat vas deferens

- Fluoxetine treatment is able to induce ejaculatory disorders;
- Influence of fluoxetine on sympathetic neurotransmission of vas deferens is not fully understood;
- The fluoxetine effects on the sympathetic neurotransmission of rat vas deferens were studied by different approaches;
- Fluoxetine treatment induced inhibitory effects on sympathetic neurotransmission of the rat vas deferens;
- Results support fluoxetine as a promising drug for the treatment of premature ejaculation.

It is described that fluoxetine treatment is able to induce ejaculatory disorders. However, the exact mechanism is still not fully understood. Therefore, this study was carried out to further evaluate the anti-ejaculatory effects of fluoxetine, using different approaches (in vitro or in vivo treatments), on the sympathetic neurotransmission of the rat vas deferens. Vas deferens from male Wistar rats were used to check the in vitro effects of fluoxetine 10− 6 M, 3.10− 6 M or 10− 5 M. Animals were also acutely (20 mg/kg, i.p. 4 h or 24 h) or chronically (10 mg/kg, i.p., 30 days) treated with fluoxetine or drug-free vehicle. The vas deferens from non-treated and treated animals were isolated and mounted in an isolated organ bath for the study of the contractions induced by adrenergic agonists, tyramine, 5-HT, Ca2 + or electrical field stimulation. In vitro or acute treatment with fluoxetine decreased the contraction induced by agonists, Ca2 + or electrical field stimulation. The chronic treatment with fluoxetine decreased the contractions induced agonists, tyramine or Ca2 +, but did not modify the contractions induced by electrical field stimulation. We have shown that in vitro or in vivo fluoxetine treatment is able to alter the sympathetic neurotransmission of the rat vas deferens which could be related to alterations in the calcium signalling.