Abstract

The role of the sympathetic adrenergic system in mediating the constant tone of penile flaccidity and returning the erect penis to its flaccid state is fairly well established. However, it is not yet known whether additional nonadrenergic-noncholinergic transmitters are involved in this process. Arginine-vasopressin (AVP, ADH), a pituitary peptide hormone with potent vasoconstrictor activity, may be one of the factors contributing to such control. The present study was undertaken to determine whether or not plasma levels of AVP change during penile flaccidity, tumescence, rigidity, and detumescence. We determined the plasma levels of AVP in the systemic as well as the cavernous blood of 25 healthy adult male volunteers who were exposed to visual and tactile erotic stimuli in order to elicit penile tumescence and erection. Whole blood was aspirated from the corpus cavernosum and the cubital vein, and AVP was quantified in plasma aliquots obtained from the whole blood samples. A marked decline in mean AVP plasma levels from 5.4+/-2.7 ng/l during flaccidity to 2.9+/-2.5 ng/l during rigidity was registered in the systemic blood of the subjects. No further decline was observed when the rigid penis became detumescent. In contrast, no alterations in AVP plasma levels were detected in the cavernous blood under the different penile conditions. The results from our study are contrary to the hypothesis of a local release and uptake of AVP in the cavernous compartment in the control of penile flaccidity and detumescence. Moreover, our findings are not in favour of AVP as an important mediator involved in adrenergic neurotransmission in the corpus cavernosum penis. Nevertheless, our data indicate that the decrease in systemic AVP levels in response to sexual arousal might be a prerequisite to facilitate penile tumescence and rigidity in healthy males.

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