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NIH Public AccessAuthor ManuscriptUrology. Author manuscript; accessible in PMC 2014 July 01.Published in final edited kind as: Urology. 2013 July ; 82(1): . doi:10.1016/j.urology.2013.04.009.NIH-PA Author Manuscript NIH-PA Author Manuscript NIH-PA Author ManuscriptAnalysis of Erectile Responses to Phospholipase A Inhibitor site imatinib inside the RatEdward A. Pankey, George F. Lasker, Serap Gur, Wayne J. G. Hellstrom, and Philip J. Kadowitz Department of Pharmacology, Tulane University School of Medicine, New Orleans, LA; as well as the Department of Urology, Tulane University College of Medicine, New Orleans, LAAbstractOBJECTIVE–To investigate the erectile and cardiovascular responses to the tyrosine kinase inhibitor imatinib inside the rat. Supplies AND METHODS–The impact of intracavernosal injection of imatinib on the intracavernosal stress (ICP), ICP/mean arterial pressure (MAP) ratio, area below the curve, and duration with the boost in ICP as well as the effect of intravenous injection of imatinib around the MAP, cardiac output, and total peripheral resistance had been investigated. The impact of the nitric oxide synthase inhibitor NG-nitro-L-arginine methyl ester on the responses to imatinib was investigated. RESULTS–Intracavernosal injection of imatinib produced substantial dose-related increases in the ICP, ICP/MAP ratio, area beneath the curve, and duration in the boost in ICP and decreases in the MAP. The erectile responses to imatinib had been fast in onset and short in duration. The erectile responses to imatinib were not drastically altered by NG-nitro-L-arginine methyl ester or cavernosal nerve crush injury, and imatinib was significantly significantly less potent than the nitric oxide donor sodium nitroprusside in inducing erection. Intravenous injection of imatinib produced significant dose-related decreases within the MAP without the need of drastically changing the cardiac output, and imatinib was considerably less potent than sodium nitroprusside in decreasing the MAP. Systemic vascular resistance was decreased within a significant dose-related manner, as well as the vasodilator responses to imatinib weren’t altered by NG-nitro-L-arginine methyl ester. CONCLUSION–The present results have indicated that imatinib has significant erectile and systemic vasodilator activity inside the rat that is certainly not dependent on nitric oxide release. A different tyrosine kinase inhibitor, nilotinib, also improved the ICP and decreased the MAP inside the rat. These data.