Baylis C, Qiu C
Department of Physiology, West Virginia University, Morgantown, USA.
Kidney Int. 1996 Jun;49(6):1727-31. doi: 10.1038/ki.1996.256.
The kidney vasculature is under tonic control by nitric oxide (NO) and in cortex, NO controls RA and Kf. Systemic NO inhibition leads to systemic hypertension, increases in RE, mediated by Ang II and ET, and direct effects on RA and Kf. The relationship between NO and other vasoconstrictor systems is variable. In the conscious relaxed animal, vasoconstrictor activity is low, yet acute NO inhibition leads to pressor and renal vasoconstrictor responses. At physiologic levels, ET unexpectedly is a renal vasodilator, possibly via NO generation at RA. When vasoconstrictor activity is high, NO is very important in maintenance of renal perfusion. Chronic L-NAME produces dose dependent systemic and glomerular capillary hypertension and eventual proteinuria and glomerular damage. NO deficiency is key in this process, although the hypertension becomes refractory to L-arginine administration and dependent on Ang II and the SNS, by mechanisms not yet defined. In contrast, the renal vasculature remains fully responsive to L-arginine, suggesting that pressor and renal vascular responses to chronic NO inhibition are separately regulated. NO generated from iNOS does not normally control BP or renal hemodynamics. The relative contributions of NO from bNOS and eNOS, and importance of NOS in different locations in the kidney, remain to be determined.
肾血管系统受一氧化氮（NO）的紧张性控制，在肾皮质中，NO控制肾血浆流量（RA）和滤过系数（Kf）。全身性NO抑制会导致全身性高血压，由血管紧张素II（Ang II）和内皮素（ET）介导的肾血浆流量增加，以及对RA和Kf的直接影响。NO与其他血管收缩系统之间的关系是可变的。在清醒放松的动物中，血管收缩活性较低，但急性NO抑制会导致升压和肾血管收缩反应。在生理水平上，ET出人意料地是一种肾血管舒张剂，可能是通过在肾血浆流量处生成NO。当血管收缩活性较高时，NO在维持肾灌注方面非常重要。慢性给予左旋精氨酸甲酯（L-NAME）会产生剂量依赖性的全身性和肾小球毛细血管高血压，最终导致蛋白尿和肾小球损伤。NO缺乏是这一过程的关键，尽管高血压对L-精氨酸给药变得难治，并依赖于Ang II和交感神经系统（SNS），但其机制尚未明确。相比之下，肾血管系统对L-精氨酸仍有充分反应，这表明对慢性NO抑制的升压和肾血管反应是分别调节的。诱导型一氧化氮合酶（iNOS）产生的NO通常不控制血压或肾血流动力学。来自组成型一氧化氮合酶（bNOS）和内皮型一氧化氮合酶（eNOS）的NO的相对贡献，以及一氧化氮合酶在肾脏不同部位的重要性，仍有待确定。
