Török J
Institute of Normal and Pathological Physiology, Slovak Academy of Sciences, Bratislava, Slovak Republic.
Physiol Res. 2008;57(6):813-825. doi: 10.33549/physiolres.931581.
This review concerns the role of nitric oxide (NO) in the pathogenesis of different models of experimental hypertension (NO-deficient, genetic, salt-dependent), which are characterized by a wide range of etiology. Although the contribution of NO may vary between different models of hypertension, a unifying characteristic of these models is the presence of oxidative stress that participates in the maintenance of elevated arterial pressure and seems to be a common denominator underlying endothelial dysfunction in various forms of experimental hypertension. Besides the imbalance between the endothelial production of vasorelaxing and vasoconstricting compounds as well as the relative insufficiency of vasodilator systems to compensate augmented vasoconstrictor systems, there were found numerous structural and functional abnormalities in blood vessels and heart of hypertensive animals. The administration of antihypertensive drugs, antioxidants and NO donors is capable to attenuate blood pressure elevation and to improve morphological and functional changes of cardiovascular system in some but not all hypertensive models. The failure to correct spontaneous hypertension by NO donor administration reflects the fact that sympathetic overactivity plays a key role in this form of hypertension, while NO production in spontaneously hypertensive rats might be enhanced to compensate increased blood pressure. A special attention should be paid to the modulation of sympathetic nervous activity in central and peripheral nervous system. These results extend our knowledge on the control of the balance between NO and reactive oxygen species production and are likely to be a basis for the development of new approaches to the therapy of diseases associated with NO deficiency.
本综述关注一氧化氮（NO）在不同实验性高血压模型（NO缺乏型、遗传型、盐依赖性型）发病机制中的作用，这些模型具有广泛的病因。尽管NO在不同高血压模型中的作用可能有所不同，但这些模型的一个共同特征是存在氧化应激，氧化应激参与维持动脉血压升高，并且似乎是各种形式实验性高血压中内皮功能障碍的一个共同因素。除了内皮产生的血管舒张和血管收缩化合物之间的失衡以及血管舒张系统相对不足以补偿增强的血管收缩系统外，在高血压动物的血管和心脏中还发现了许多结构和功能异常。在一些但并非所有高血压模型中，给予抗高血压药物、抗氧化剂和NO供体能够减轻血压升高，并改善心血管系统的形态和功能变化。通过给予NO供体未能纠正自发性高血压，这反映出交感神经过度活跃在这种高血压形式中起关键作用，而自发性高血压大鼠中的NO生成可能会增强以补偿血压升高。应特别关注中枢和外周神经系统中交感神经活动的调节。这些结果扩展了我们对NO与活性氧生成之间平衡控制的认识，并且可能成为开发与NO缺乏相关疾病新治疗方法的基础。
