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首页> 外文期刊>Life sciences >Angiotensin II type 1 (AT1)-receptor blocker prevents impairment of endothelium-dependent cerebral vasodilation by acute cigarette smoking in rats.
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Angiotensin II type 1 (AT1)-receptor blocker prevents impairment of endothelium-dependent cerebral vasodilation by acute cigarette smoking in rats.

机译：血管紧张素II 1型（AT1）受体阻滞剂可防止大鼠急性吸烟引起内皮依赖性脑血管舒张损伤。

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Our aim was to test for smoking-induced endothelial dysfunction in rat cerebral vessels, then to evaluate the effect of valsartan [angiotensin II type I (AT1)-receptor blocker] on that impairment. In pentobarbital-anesthetized, mechanically ventilated Sprague-Dawley rats, we used a cranial window preparation to measure changes in pial vessel diameters following topical applications of acetylcholine (Ach) (before and after smoking or intravenous nicotine infusion; n = 6 in each group), and adenosine (n = 6 for before and after smoking). Then, after intravenous valsartan pretreatment we reexamined the pial vasodilator response to topical Ach (before and after cigarette smoking). Under control conditions, cerebral arterioles were dilated by 6.9 +/- 4.2% and 13.6 +/- 4.8% by topical Ach (10(-6) M and 10(-5) M, respectively) and by 6.4 +/- 2.5% and 12.2 +/- 3.1% by topical adenosine (10(-5) M and 10(-4) M, respectively). One hour after a 1-min inhalation of mainstream smoke (1-mg nicotine cigarette), 10(-5)M Ach constricted cerebral arterioles (-4.4 +/- 4.1%), while 10(-4) M adenosine dilated them by 13.4 +/- 3.4%. One hour after a 1-min nicotine infusion (0.05 mg), 10(-5) M Ach dilated cerebral arterioles by 9.9 +/- 2.4%. Thus, vasodilator response to topical Ach was impaired after smoking, whereas that to adenosine was unaffected. However, the vasodilator response to Ach was unaffected by intravenous nicotine. Valsartan prevented smoking from impairing Ach-induced vasodilation. In conclusion, acute single-cigarette smoking causes a dysfunction of endothelium-dependent, but not endothelium-independent, vasodilation of rat cerebral vessels in vivo, and the effect was not mimicked by intravenous nicotine. AT1-receptor blockade prevented the above smoking-induced impairment of endothelium-dependent vasodilation.
机译：我们的目的是测试吸烟引起的大鼠脑血管内皮功能障碍，然后评估缬沙坦[I型血管紧张素II（AT1）-受体阻滞剂]对该损伤的影响。在戊巴比妥麻醉的，机械通气的Sprague-Dawley大鼠中，我们使用了颅窗制剂来测量局部应用​​乙酰胆碱（Ach）后（吸烟或静脉内尼古丁输注之前和之后;每组n = 6）的瞳孔血管直径的变化。和腺苷（吸烟前后n = 6）。然后，在进行静脉缬沙坦预处理后，我们重新检查了对局部Ach（在吸烟前后）的乳头血管舒张反应。在对照条件下，局部Ach（分别为10（-6）M和10（-5）M）将脑小动脉扩张6.9 +/- 4.2％和13.6 +/- 4.8％，再扩张6.4 +/- 2.5％和12.2 +/- 3.1％的局部腺苷（分别为10（-5）M和10（-4）M）。吸入主流烟气（1-mg尼古丁烟）1分钟后一小时，10（-5）M Ach收缩性脑小动脉（-4.4 +/- 4.1％），而10（-4）M腺苷则通过13.4 +/- 3.4％。尼古丁注入1分钟（0.05 mg）后一小时，将10（-5）M Ach扩张的脑小动脉降低9.9 +/- 2.4％。因此，吸烟后血管舒张剂对局部Ach的反应减弱，而对腺苷的舒张反应则不受影响。但是，对Ach的血管舒张反应不受静脉内尼古丁的影响。缬沙坦可防止吸烟损害Ach引起的血管舒张。总之，急性单支香烟吸烟会在体内引起大鼠脑血管的内皮依赖性（而非内皮依赖性）血管舒张功能障碍，静脉内尼古丁不能模仿这种作用。 AT1受体阻滞阻止了上述吸烟诱导的内皮依赖性血管舒张损害。

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