{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,3,19]],"date-time":"2025-03-19T07:10:03Z","timestamp":1742368203396,"version":"3.40.1"},"reference-count":22,"publisher":"Wiley","issue":"4","license":[{"start":{"date-parts":[[2012,1,24]],"date-time":"2012-01-24T00:00:00Z","timestamp":1327363200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"name":"\u00c7ukurova University Research Foundation","award":["TF 2009 BAP3"],"award-info":[{"award-number":["TF 2009 BAP3"]}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Neurourology and Urodynamics"],"published-print":{"date-parts":[[2012,4]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:sec><jats:title>Aims<\/jats:title><jats:p>The effect of a non\u2010specific thiol\u2010alkylating agent<jats:italic>N<\/jats:italic>\u2010ethylmaleimide (NEM) was studied on neurogenic contractile mechanisms in rat ventral prostate gland.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>Male Wistar albino rats were used. The rats were killed by cervical dislocation under sevoflurane anesthesia and ventral prostate gland was removed. Two preparations were obtained from each lobe. Neurally evoked isometric contractions were induced using trains of electrical field stimulation (EFS; 0.5, 1, 4, or 8\u2009Hz). The effect of NEM on the contractions to EFS was examined in the absence or presence of adrenergic and\/or purinergic antagonists.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>NEM enhanced the EFS\u2010evoked contractions without altering the basal tone. These effects were significantly suppressed by an \u03b1<jats:sub>1<\/jats:sub>\u2010adrenergic receptor antagonist (prazosin), a P2\u2010purinergic antagonist (suramin), a specific P2X\u2010receptor antagonist pyridoxal\u2010phosphate\u20106\u2010azophenyl\u20102\u2032,4\u2032\u2010disulfonate (PPADS), an ATP analog (\u03b1,\u03b2\u2010methylene ATP), or a calcium channel blocker (verapamil). This facilitating effect of NEM did not occur following the administration of<jats:sc>L<\/jats:sc>\u2010cysteine or glutathione which saturated NEM with excess thiols. However, a thiol\u2010oxidant diamide failed to affect the contractions to EFS. An adrenergic neuron blocker (guanethidine) completely suppressed the responses to NEM. On the other hand, an \u03b1<jats:sub>2<\/jats:sub>\u2010adrenergic receptor blocker (yohimbine), a nitric oxide synthase inhibitor (<jats:italic>N<\/jats:italic><jats:sup><jats:italic>\u03c9<\/jats:italic><\/jats:sup>\u2010nitro\u2010<jats:sc>L<\/jats:sc>\u2010arginine) or a cholinergic muscarinic receptor antagonist (atropine) did not significantly affect the facilitatory response of NEM.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusions<\/jats:title><jats:p>These findings suggest that NEM has a prejunctional facilitatory action on the adrenergic nerves in rat prostate tissue to enhance release of transmitters, noradrenaline, and ATP. NEM sensitive proteins involved in transmitter release mechanisms can play a role in this effect. Neurourol. 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