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NIH Public AccessAuthor ManuscriptUrology. Author manuscript; readily available in PMC 2014 July 01.Published in final edited form as: Urology. 2013 July ; 82(1): . doi:ten.1016/j.urology.2013.04.009.NIH-PA Author Manuscript NIH-PA Author Manuscript NIH-PA Author ManuscriptAnalysis of Erectile Responses to Imatinib inside the RatEdward A. Pankey, George F. Lasker, Serap Gur, Wayne J. G. Hellstrom, and Philip J. Kadowitz Division of Pharmacology, Tulane University College of Medicine, New Orleans, LA; and the Department of Urology, Tulane University College of Medicine, New Orleans, LAAbstractOBJECTIVE–To investigate the erectile and cardiovascular responses towards the tyrosine kinase inhibitor imatinib within the rat. Supplies AND METHODS–The effect of intracavernosal injection of imatinib around the intracavernosal pressure (ICP), ICP/mean arterial stress (MAP) ratio, location under the curve, and duration of the boost in ICP and also the impact of intravenous injection of imatinib on the MAP, cardiac output, and total peripheral resistance have been investigated.(S)-4-(1-Aminoethyl)phenol hydrobromide Price The effect from the nitric oxide synthase inhibitor NG-nitro-L-arginine methyl ester around the responses to imatinib was investigated.Exatecan (mesylate) Chemical name RESULTS–Intracavernosal injection of imatinib produced substantial dose-related increases within the ICP, ICP/MAP ratio, location under the curve, and duration with the improve in ICP and decreases within the MAP. The erectile responses to imatinib were fast in onset and quick in duration. The erectile responses to imatinib were not substantially altered by NG-nitro-L-arginine methyl ester or cavernosal nerve crush injury, and imatinib was considerably significantly less potent than the nitric oxide donor sodium nitroprusside in inducing erection.PMID:23074147 Intravenous injection of imatinib created significant dose-related decreases within the MAP without having considerably altering the cardiac output, and imatinib was substantially much less potent than sodium nitroprusside in decreasing the MAP. Systemic vascular resistance was decreased in a considerable dose-related manner, and the vasodilator responses to imatinib had been not altered by NG-nitro-L-arginine methyl ester. CONCLUSION–The present final results have indicated that imatinib has substantial erectile and systemic vasodilator activity in the rat which is not dependent on nitric oxide release. An additional tyrosine kinase inhibitor, nilotinib, also increased the ICP and decreased the MAP in the rat. These.
