Ischaemia-reperfusion damage induced by torsion/detorsion of the testicles may be a causative factor leading to erectile dysfunction through oxidative stress-dependent changes in the responses of the penile bulb, an erectile tissue of the penis. We aimed at investigating the effects of unilateral testicular torsion/detorsion (2 or 24 hr) treatment on relaxations induced by electrical field stimulation and sodium nitroprusside in rat isolated penile bulb. Male Sprague-Dawley rats used in the study were divided into two groups. The treatment group was subjected to unilateral torsion followed by detorsion for 2 or 24 hr, while the control group underwent only sham operation. For in vitro organ bath experiments, penile bulbs were isolated and responses to relaxant agents and electrical field stimulation (70 V, 1 msec., 0.5 -8 Hz, 5 sec.) were recorded on a computer-based data acquisition system via a force displacement transducer. In tissues precontracted with phenylephrine (3 × 10 -6 M), relaxations induced by electrical field stimulation were not significantly different before and after 2 or 24 hr of detorsion. Similarly sodium nitroprusside-(10 -8 -3 × 10 -6 M) and papaverine-induced (10 -7 -10 -4 M) relaxations were also found unchanged in the detorsion group compared to control. In conclusion, spermatic cord torsion did not lead to impairment in nitric oxide-mediated relaxant responses of the rat isolated penile bulb.The penile bulb is the proximal part of corpus spongiosum which structure greatly varies within mammals. Canine and rat penile bulbs have nitric oxide synthase-containing nerve fibres that are assumed to play an important role in initiating the erection of glans penis [1,2]. Thus, an alteration in the function of these nerves may in part be a causative factor leading to erectile dysfunction.Unilateral testicular torsion is a medical emergency caused by torsion of the spermatic cord and is treated by surgical detorsion [3]. After unilateral torsion, the blood flow in both ipsilateral and contralateral internal spermatic arteries decrease [4][5][6], which subsequently leads to testicular ischaemia. The mechanisms of this phenomenon have been ascribed to direct damage caused by ischaemia during torsion and to a secondary effect due to reperfusion arising from detorsion [6,7]. Ischaemia reperfusion injury has been associated with the overgeneration of reactive oxygen and nitrogen species [8]. In our previous study, we found that oxygen-free radicals reduced nitrergic nerve-mediated relaxant responses only in the presence of an inhibitor of endogenous Cu/Zn superoxide dismutase in rat penile bulb [9]. Besides, we have recently demonstrated that unilateral testicular torsion in the rat reduces neurotransmitter release from nerve terminals in the ipsilateral vas deferens [7]. Moreover, a recent report provides evidence for a link between testicular torsion and erectile dysfunction [10]. Thus, it remains to be determined whether unilateral testicular torsion/detorsion treatment might also influen...