正常、高血压和易中风大鼠的脑一氧化氮合酶活性

Brain nitric oxide synthase activity in normal, hypertensive, and stroke-prone rats.

作者信息

Clavier N, Tobin J R, Kirsch J R, Izuta M, Traystman R J

机构信息

Department of Anesthesiology and Critical Care Medicine, Johns Hopkins Medical Institutions, Baltimore, Md.

出版信息

Stroke. 1994 Aug;25(8):1674-7; discussion 1677-8. doi: 10.1161/01.str.25.8.1674.

DOI:10.1161/01.str.25.8.1674

PMID:7518973

Abstract

BACKGROUND AND PURPOSE

Nitric oxide-mediated cerebral vasodilation is altered in spontaneously hypertensive stroke-prone rats. Stroke predisposition in this strain could be related to a genetic defect of brain nitric oxide synthase, the enzyme responsible for nitric oxide production. We tested the hypothesis that brain nitric oxide synthase activity is altered in spontaneously hypertensive stroke-prone rats compared with spontaneously hypertensive or Wistar-Kyoto rats.

METHODS

A colony of spontaneously hypertensive stroke-prone rats was bred, in which the rate of neurological events under salt load was assessed. In a separate cohort of animals brain nitric oxide synthase activity was measured in spontaneously hypertensive stroke-prone rats (n = 6) and in spontaneously hypertensive (n = 6) and genetically related Wistar-Kyoto rats (n = 6). Calcium dependency of nitric oxide synthase was also assessed in cortical brain samples from the three rat strains to determine if altered calcium-dependent activation of nitric oxide synthase was present.

RESULTS

Brain nitric oxide synthase activity was highest in the cerebellum (eg, spontaneously hypertensive stroke-prone rats: cerebral cortex, 10.6 +/- 0.9; cerebellum, 50.1 +/- 12.0; brain stem, 14.7 +/- 10.3 pmol/mg protein per minute); however, there was no difference among the three rat strains in any region (eg, cerebral cortex: spontaneously hypertensive stroke-prone, 10.6 +/- 0.9; spontaneously hypertensive, 10.8 +/- 0.5; Wistar-Kyoto, 10.9 +/- 0.7 pmol/mg protein per minute) or at any calcium concentration tested.

CONCLUSIONS

A genetic defect of brain nitric oxide synthase is unlikely to be the cause of stroke predisposition in spontaneously hypertensive stroke-prone rats.

摘要

背景与目的

在自发性高血压易中风大鼠中，一氧化氮介导的脑血管舒张功能发生改变。该品系的中风易感性可能与脑一氧化氮合酶的基因缺陷有关，脑一氧化氮合酶是负责产生一氧化氮的酶。我们检验了这样一个假设，即与自发性高血压大鼠或Wistar - Kyoto大鼠相比，自发性高血压易中风大鼠的脑一氧化氮合酶活性发生了改变。

方法

培育了一群自发性高血压易中风大鼠，评估了盐负荷下神经事件的发生率。在另一组动物中，测量了自发性高血压易中风大鼠（n = 6）、自发性高血压大鼠（n = 6）和基因相关的Wistar - Kyoto大鼠（n = 6）的脑一氧化氮合酶活性。还评估了来自这三种大鼠品系的大脑皮质样本中一氧化氮合酶的钙依赖性，以确定是否存在一氧化氮合酶钙依赖性激活的改变。

结果

脑一氧化氮合酶活性在小脑中最高（例如，自发性高血压易中风大鼠：大脑皮质，10.6±0.9；小脑，50.1±12.0；脑干，14.7±10.3 pmol/mg蛋白每分钟）；然而，在任何区域（例如，大脑皮质：自发性高血压易中风大鼠，10.6±0.9；自发性高血压大鼠，10.8±0.5；Wistar - Kyoto大鼠，10.9±0.7 pmol/mg蛋白每分钟）或任何测试的钙浓度下，这三种大鼠品系之间均无差异。