Department of Pharmacology, Shiga University of Medical Science, Otsu, Japan.
J Hypertens. 2009 Oct;27(10):1929-40. doi: 10.1097/HJH.0b013e32832e8ddf.
Nitric oxide formed by neuronal nitric oxide synthase (nNOS) in the brain, autonomic inhibitory (nitrergic) nerves, and heart plays important roles in the control of blood pressure. Activation of nitrergic nerves innervating the systemic vasculature elicits vasodilatation, decreases peripheral resistance, and lowers blood pressure. Impairment of nitrergic nerve function, as well as endothelial dysfunction, results in systemic and pulmonary hypertension and decreased regional blood flow. Blockade of nNOS activity in the brain, particularly the medulla and hypothalamus, causes systemic hypertension. Under hypertensive states, such as those in spontaneously hypertensive and Dahl salt-sensitive rats, the expression of the nNOS gene in the brain is increased; this appears to counteract the activated sympathetic function in the vasomotor center. The present article summarizes information concerning the modulation of systemic and pulmonary hypertension through nNOS-derived nitric oxide produced in the brain and periphery.
由脑内神经元型一氧化氮合酶(nNOS)、自主抑制(nitrergic)神经和心脏产生的一氧化氮在血压控制中发挥重要作用。激活支配全身血管的nitrergic 神经可引起血管舒张、外周阻力降低和血压下降。nitrergic 神经功能障碍以及内皮功能障碍可导致全身和肺动脉高压以及局部血流减少。脑内 nNOS 活性的阻断,特别是在延髓和下丘脑,可导致全身高血压。在高血压状态下,如自发性高血压和 Dahl 盐敏感大鼠中,脑内 nNOS 基因的表达增加;这似乎抵消了血管运动中枢中激活的交感功能。本文总结了通过脑内和外周产生的 nNOS 衍生的一氧化氮调节全身和肺动脉高压的信息。