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首页> 外文期刊>The journal of sexual medicine >NO-donating oximes relax corpora cavernosa through mechanisms other than those involved in arterial relaxation
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NO-donating oximes relax corpora cavernosa through mechanisms other than those involved in arterial relaxation

机译：不含NO的肟通过不同于动脉舒张的机制舒缓海绵体

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Introduction: Erectile dysfunction (ED), as well as many cardiovascular diseases, is associated with impaired nitric oxide (NO) bioavailability. Recently, oxime derivatives have emerged as vasodilators due to their NO-donating capacities. However, whether these oximes offer therapeutic perspectives as an alternative NO delivery strategy for the treatment of ED is unexplored. Aims: This study aims to analyze the influence of formaldoxime (FAL), formamidoxime (FAM), and cinnamaldoxime (CAOx) on corporal tension and to elucidate the underlying molecular mechanisms. Methods: Organ bath studies were carried out measuring isometric tension on isolated mice corpora cavernosa (CC), thoracic aorta, and femoral artery. After contraction with norepinephrine (NOR), cumulative concentration-response curves of FAL, FAM, and CAOx (100nmol/L-1mmol/L) were performed. Main Outcome Measures: FAL-/FAM-induced relaxations were evaluated in the absence/presence of various inhibitors of different molecular pathways. Results: FAL, FAM, and CAOx relax isolated CC as well as aorta and femoral artery from mice. ODQ (soluble guanylyl cyclase-inhibitor), diphenyliodonium chloride (nonselective flavoprotein inhibitor), and 7-ethoxyresorufin (inhibitor of CYP450 1A1 and NADPH-dependent reductases) substantially blocked the FAL-/FAM-induced relaxation in the arteries but not in CC. Only a small inhibition of the FAM response in CC was observed with ODQ. Conclusions: This study shows for the first time that NO-donating oximes relax mice CC. Therefore, oximes are a new group of molecules with potential for the treatment of ED. However, the underlying mechanism(s) of the FAL-/FAM-induced corporal relaxation clearly differ(s) from the one(s) involved in arterial vasorelaxation.
机译：简介：勃起功能障碍（ED）以及许多心血管疾病与一氧化氮（NO）生物利用度受损有关。近来，肟衍生物由于其NO-给体能力而出现为血管扩张剂。然而，这些肟是否提供治疗观点作为治疗ED的另一种NO释放策略尚待探讨。目的：本研究旨在分析福尔多肟（FAL），甲酰胺肟（FAM）和肉桂醛肟（CAOx）对体张力的影响，并阐明其潜在的分子机制。方法：对分离的小鼠海绵体（CC），胸主动脉和股动脉进行等离子浴张力测量。用去甲肾上腺素（NOR）收缩后，进行FAL，FAM和CAOx（100nmol / L-1mmol / L）的累积浓度-响应曲线。主要结果指标：在不同分子途径的各种抑制剂存在/不存在下，评估FAL // FAM引起的松弛。结果：FAL，FAM和CAOx使小鼠分离的CC以及主动脉和股动脉松弛。 ODQ（可溶性鸟苷酰环化酶抑制剂），二苯基碘化氯化物（非选择性黄素蛋白抑制剂）和7-乙氧基苯丁三醇（CYP450 1A1抑制剂和NADPH依赖性还原酶）基本上阻断了FAL- / FAM诱导的动脉舒张，但未阻断CC。用ODQ仅观察到CC中FAM应答的少量抑制。结论：这项研究首次表明，捐赠NO的肟使小鼠CC松弛。因此，肟是具有治疗ED潜力的一组新分子。然而，FAL // FAM引起的体表松弛的潜在机制与参与动脉血管舒张的机制明显不同。

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