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We investigated whether bacterial lipopolysaccharide (LPS) treatment causes any hyporeactivity in rat vas deferens tissue and also whether vitamin E or sodium selenate has any restorative effect on this possible hyporesponsiveness. LPS treatment attenuated contractions to electrical field stimulation (EFS), phenylephrine, or ATP at the prostatic and epididymal ends. Treatment with the inducible nitric oxide synthase (iNOS) inhibitor aminoguanidine or vitamin E could prevent the impairment in contractile responses of both ends to EFS and phenylephrine but sodium selenate could restore these impaired contractions at only the epididymal end. LPS treatment also caused a similar significantly impairment on purinergic or adrenergic component of nerve-evoked contractions in the presence of prazosin or suramin, respectively, and vitamin E or sodium selenate could restored this impairment at both ends. On the other hand, both antioxidant agents failed to restore the impaired ATP-induced contractions in LPS-treated rats at both ends. In conclusion, LPS-treatment caused a hyporeactivity in the rat vas deferens. A possible increased oxidative activity in the vas deferens may be a major reason for the impairment of contractile responses. The restorative effects of vitamin E and/or sodium selenate on this hypocontractility may depend on their antioxidant properties or their inhibitory action on the iNOS.

We studied the effect of vitamin E and sodium selenate treatment on the neurogenic and endothelium-dependent relaxation of isolated corpus cavernosum obtained from streptozotocin-induced diabetic mice. Relaxant responses of corpus cavernosum precontracted by phenylephrine to electrical field stimulation and to acetylcholine were significantly decreased in diabetic mice. There was no significant difference between diabetic and non-diabetic groups for the relaxant response of corpus cavernosum to sodium nitroprusside and papaverine. Treatment with sodium selenate, but not vitamin E, partially prevented the impairment of the neurogenic relaxation, whereas both had a significant, partial restorative action on endothelial dysfunction in corpus cavernosum obtained from diabetic groups. Neither agent exhibited a significant action on the relaxant responses of corpus cavernosum obtained from non-diabetic mice. A decrease in the sensitivity of the neurogenic impairment to antioxidant action may develop more rapidly than that of endothelial dysfunction in streptozotocin-induced diabetic mice.