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The potential of stimulating nitric oxide formation in the treatment of hypertension

机译:在高血压治疗中刺激一氧化氮形成的潜力

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Introduction: Hypertension is a leading cause of morbidity and mortality worldwide. A major pathophysiological factor contributing to hypertension is reduced nitric oxide (NO) bioavailability. Strategies to address this pathophysiological mechanism could offer significant advantages.Areas covered: In this review we aimed at examining a variety of drugs (statins, beta-adrenergic receptor blockers, calcium channel blockers, angiotensin converting enzyme inhibitors, angiotensin II type-1 receptor blockers) used to treat hypertension and other cardiovascular diseases, particularly with respect to their potential of increasing NO bioavailability and activity in the cardiovascular system. There is now evidence supporting the notion that many cardiovascular drugs activate NO signaling or enhance NO bioavailability as a contributing mechanism to their beneficial cardiovascular effects. Moreover, other drugs may attenuate NO inactivation by superoxide and other reactive oxygen species by exerting antioxidant effects. More recently, the NO oxidation products nitrite and nitrate have been acknowledged as sources of NO after recycling back to NO. Activation of the nitrate-nitrite-NO pathway is an alternate pathway that may generate NO from both anions and exert antihypertensive effects.Expert opinion: In this review, we provide an overview of the possible mechanisms by which these drugs enhance NO bioavailability and help in the therapy of hypertension.
机译:介绍:高血压是全世界发病率和死亡率的主要原因。有助于高血压的主要病理生理因素减少了一氧化氮(NO)生物利用度。解决这种病理生理机制的策略可以提供显着的优势。涉及涵盖的优势:在本综述中,我们旨在检查各种药物(他汀类药物,β-肾上腺素能受体阻滞剂,钙通道阻滞剂,血管紧张素转换酶抑制剂,血管紧张素II型受体阻滞剂)用于治疗高血压和其他心血管疾病,特别是对于在心血管系统中不增加生物利用度和活性的潜力。现在有证据表明,支持许多心血管药物的概念激活无信号或提高生物利用度,作为其有益心血管作用的贡献机制。此外,其他药物可以通过施加抗氧化效应来衰减超氧化物和其他活性氧物质的灭活。最近,没有氧化产物亚硝酸盐和硝酸盐已被视为在回收回到NO后的NO源。硝酸亚硝酸盐 - NO途径的活化是可以从阴离子产生的替代途径,并发挥抗高血压作用。普及意见:在本次审查中,我们概述了这些药物增强无生物利用度和帮助的可能机制概述高血压的治疗。

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