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乙醇对一氧化氮合成抑制所引起的升压反应的抑制作用。

Suppression by ethanol of pressor response caused by the inhibition of nitric oxide synthesis.

作者信息

Wang Y X, Pang C C

机构信息

Department of Pharmacology and Therapeutics, Faculty of Medicine, University of British Columbia, Vancouver, Canada.

出版信息

Eur J Pharmacol. 1993 Mar 23;233(2-3):275-8. doi: 10.1016/0014-2999(93)90061-l.

DOI:10.1016/0014-2999(93)90061-l
PMID:8467873
Abstract

The effects of ethanol on mean arterial pressure (MAP) and heart rate (HR) responses to the nitric oxide synthase inhibitor, NG-nitro-L-arginine, and to angiotensin II and noradrenaline were studied in rats. I.V. bolus injections of NG-nitro-L-arginine dose dependently increased MAP in vehicle-pretreated rats, with a maximum increase of 56 +/- 7 mm Hg and an ED50 of 3.8 +/- 0.4 mg/kg, respectively. I.v. infusions of ethanol dose dependently reduced maximum MAP response to NG-nitro-L-arginine, with a Ki of 96 +/- 8 mg/kg per min but did not alter the ED50. Ethanol (48 mg/kg per min) did not modify the MAP response to i.v. bolus injections of angiotensin II (0.02-1.28 micrograms/kg) or noradrenaline (0.25-16 micrograms/kg). However, ethanol attenuated the reflex HR responses of NG-nitro-L-arginine and angiotensin II but not that of noradrenaline. The results demonstrate that ethanol selectively but non-competitively inhibits the MAP response to NG-nitro-L-arginine, suggesting an interaction between ethanol and the L-arginine/nitric oxide pathway.

摘要

在大鼠中研究了乙醇对平均动脉压(MAP)和心率(HR)对一氧化氮合酶抑制剂NG-硝基-L-精氨酸、血管紧张素II和去甲肾上腺素反应的影响。静脉推注NG-硝基-L-精氨酸可使预先用赋形剂处理的大鼠的MAP剂量依赖性增加,最大增加量分别为56±7 mmHg,ED50为3.8±0.4 mg/kg。静脉输注乙醇可使对NG-硝基-L-精氨酸的最大MAP反应剂量依赖性降低,Ki为96±8 mg/kg每分钟,但不改变ED50。乙醇(48 mg/kg每分钟)不改变对静脉推注血管紧张素II(0.02 - 1.28微克/千克)或去甲肾上腺素(0.25 - 16微克/千克)的MAP反应。然而,乙醇减弱了NG-硝基-L-精氨酸和血管紧张素II的反射性HR反应,但不影响去甲肾上腺素的反射性HR反应。结果表明,乙醇选择性但非竞争性地抑制对NG-硝基-L-精氨酸的MAP反应,提示乙醇与L-精氨酸/一氧化氮途径之间存在相互作用。

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