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• W2087417811 abstract "Introduction Heme oxygenase (HO) enzyme catalyzes oxidative degradation of heme to biliverdin and carbon monoxide (CO). CO shares many properties with nitric oxide (NO) including the activation of soluble guanyl cyclase. Aim To assess cavernous tissue HO activity and cyclic guanosine monophosphate (cGMP) levels in response to oral phosphodiesterse type 5 (PDE5) inhibitors. Methods Seven hundred twenty male Sprague-Dawley rats, divided into six groups, were investigated. Group 1, controls; group 2 received sildenafil citrate orally; group 3 received vardenafil hydrochloride; and group 4 received tadalafil. Group 5 was subdivided into three equal subgroups, received the same dose of each drug added to the HO inhibitor, Zn protoporphyrin. Group 6 was subdivided into three equal subgroups, received the same dose of each drug added to the NO inhibitor, L-nitroarginine methylester. Eight rats from each group/subgroup were sacrificed at 0.5, 1, 2, 3, 4, 6, 18, 24, and 36 hours, respectively. Main Outcome Measures HO enzyme activity assay and cGMP tissue levels in dissected rat cavernous tissues. Results Both cavernous tissue HO enzyme activity and cGMP levels were increased significantly in sildenafil-, vardenafil-, and tadalafil-treated rats compared with the controls, with significant decreases after either HO or NO inhibition. Cavernous tissue HO enzyme activity and cGMP showed a positive significant correlation (r = 0.854, P < 0.001). Conclusion The effects of PDE5 inhibitors in cavernous tissue are partly mediated through HO enzyme activity. Abdel Aziz MT, Mostafa T, Atta H, Rashed L, Marzouk SA, Obaia EM, Sabry D, Hassouna AA, El-Shehaby AM, and Abdel Aziz AT. The role of PDE5 inhibitors in heme oxygenase–cGMP relationship in rat cavernous tissues." @default.
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• W2087417811 date "2008-07-01" @default.
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• W2087417811 title "The Role of PDE5 Inhibitors in Heme Oxygenase–cGMP Relationship in Rat Cavernous Tissues" @default.
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• W2087417811 doi "https://doi.org/10.1111/j.1743-6109.2007.00729.x" @default.
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