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正常血压和自发性高血压大鼠肾皮质和髓质中一氧化氮合酶的活性

Nitric oxide synthase activity in renal cortex and medulla of normotensive and spontaneously hypertensive rats.

作者信息

Nava E, Llinás M T, Gonzalez J D, Salazar F J

机构信息

Departamento de Fisiologiá, Facultad de Medicina, Universidad de Murcia, Spain.

出版信息

Am J Hypertens. 1996 Dec;9(12 Pt 1):1236-9. doi: 10.1016/s0895-7061(96)00325-1.

DOI:10.1016/s0895-7061(96)00325-1
PMID:8972897
Abstract

The medullary portion of the kidney plays a crucial role in the control of sodium and water excretion and arterial pressure. This control is anomalous in hypertension and may be related to an impaired renal nitric oxide (NO) production. We have measured the activity of NO synthase (NOS) in the renal medulla, renal cortex, heart, and aorta from normotensive Wistar Kyoto rats (WKY) and spontaneously hypertensive rats (SHR). Enzyme activity was determined by measuring the conversion of 14C-L-arginine to 14C-L-citrulline. Ca2+-dependent NOS activity was considerably higher in the renal medulla than in the other tissues studied, both in WKY and SHR. The medulla and heart of the SHR displayed a higher Ca2+-dependent NOS activity compared to that of WKY. No differences were found in the Ca2+-independent NOS activity, except for the renal cortex of the SHR, which was higher than in the rest of the tissues. These observations indicate that the renal medulla has a high relative capacity to synthesize NO and suggest that the impaired renal medullary control of arterial pressure of genetic hypertension is not due to a reduced NO production by the kidney.

摘要

肾脏的髓质部分在控制钠和水的排泄以及动脉血压方面起着关键作用。这种控制在高血压中是异常的,并且可能与肾脏一氧化氮(NO)生成受损有关。我们已经测量了正常血压的Wistar Kyoto大鼠(WKY)和自发性高血压大鼠(SHR)的肾髓质、肾皮质、心脏和主动脉中一氧化氮合酶(NOS)的活性。通过测量14C-L-精氨酸向14C-L-瓜氨酸的转化来确定酶活性。在WKY和SHR中,肾髓质中Ca2+依赖性NOS活性均显著高于其他所研究的组织。与WKY相比,SHR的髓质和心脏表现出更高的Ca2+依赖性NOS活性。除了SHR的肾皮质中Ca2+非依赖性NOS活性高于其他组织外,未发现其他差异。这些观察结果表明肾髓质具有较高的合成NO的相对能力,并提示遗传性高血压中肾髓质对动脉血压的控制受损并非由于肾脏NO生成减少所致。

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