Effects of angiotensin II on NO bioavailability evaluated using a catheter-type NO sensor
Effects of angiotensin II on NO bioavailability evaluated using a catheter-type NO sensor
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DOI：
10.1161/01.hyp.0000248920.16956.d8
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发表时间：
2006-12-01
期刊：
影响因子：
8.3
通讯作者：
Akasaka, Takashi
中科院分区：
文献类型：
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作者：
Imanishi, Toshio;Kobayashi, Katsunobu;Akasaka, Takashi
我们使用导管型NO传感器研究了血管紧张素(Ang)II对注射Ang II的兔体内NO生物利用度的急性或慢性影响。雄性新西兰大白兔分别以每分钟200 ng/kg的速度注入赋形剂(Sham)、血管紧张素转换酶II(Ang II)或血管紧张素Ⅱ受体拮抗剂(Valsartan)或抗氧化剂(Tempoll)，连续24小时或14天。用置于主动脉内的导管式NO传感器测量血浆NO浓度。然后，在给予或不给予N-G-甲基-L精氨酸的情况下，向主动脉弓内注入生理盐水(赋形剂)和乙酰胆碱(ACh)。Ang II组与对照组相比，ACh引起的血浆NO水平升高明显减轻。Ang II组基础血浆NO浓度下降幅度明显低于对照组。Ang II组血浆过氧亚硝酸盐浓度显著高于对照组。血管紧张素转换酶II的负性作用，即基础和ACh诱导的NO生成减少和氧化应激增加，可被valsartan或temol共同处理显著抑制。短期应用血管紧张素转换酶II可显著增加ACh诱导的血浆NO浓度升高和基础NO释放量。虽然Ang II在短期内刺激NO的释放，但长期应用Ang II可导致血管紧张素Ⅱ输注的兔模型主动脉中NO的生物利用度降低。
We investigated the acute or chronic effects of angiotensin (Ang) II on the bioavailability of NO in Ang II-infused rabbits using the catheter-type NO sensor. Male New Zealand White rabbits were infused with vehicle (sham), Ang II at a rate of 200 ng/kg per minute, either alone or in combination with hydralazine, Ang II type I receptor antagonist (valsartan), or an antioxidant (tempol) for 24 hours or 14 days. Plasma NO concentration was measured using the catheter-type NO sensor located in the aorta. We then infused saline (vehicle) and acetylcholine (ACh) into the aortic arch with or without pretreatment with N-G-methyl-L-arginine. An increase in plasma NO levels in response to ACh was significantly attenuated in the Ang II group compared wit the control group. The decrease in the basal plasma NO concentration was significantly lower in the Ang II group than in the control group. Plasma peroxynitrite concentrations in Ang II group were significantly higher than in the control group. The negative effects of Ang II, that is, the decrease in basal and ACh-induced NO production and the increase in oxidative stress, were significantly suppressed by the cotreatment with either valsartan or tempol. Short-term treatment with Ang II significantly increased the ACh-induced increase in plasma NO concentration, as well as basal NO release. Although Ang II stimulates release of NO in the short term, chronic treatment with Ang II elicits the decreased NO bioavailability in the aorta of the Ang II-infusion rabbit model.