L-arginine restores dilator responses of the basilar artery to acetylcholine during chronic hypertension.

L-arginine restores dilator responses of the basilar artery to acetylcholine during chronic hypertension.
复制标题

L-精氨酸可恢复慢性高血压期间基底动脉对乙酰胆碱的扩张反应。

DOI:
10.1161/01.hyp.27.4.893
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发表时间:
1996
期刊:
Hypertension (Dallas, Tex. : 1979)
影响因子:
--
通讯作者:
Heistad,DD
Heistad,DD
中科院分区:
--
文献类型:
--
作者:
Kitazono,T;Faraci,FM;Heistad,DD

文献摘要

被引文献

相似文献

本研究的目的是检验一氧化氮合酶底物精氨酸的给药是否能恢复乙酰胆碱诱导的慢性高血压大鼠基底动脉扩张。通过颅窗测量6至7个月(成年)和12个月(老年)麻醉的易卒中自发性高血压大鼠(SHRSP)和血压正常的Wistar-Kyoto大鼠(WKY)的基底动脉直径。在对照条件下,SHRSP的基线基底动脉直径(成人,239±30 μm;老年人,198±13 μm)(平均值±SE)小于WKY(成人,261±10 μm;老年人,259±7 μm)(P<0.05 vs SHRSP)。局部应用乙酰胆碱(10− 5 mol/L)可使WKY基底动脉扩张,而成年和老年SHRSP的基底动脉扩张均受损(P<0.05)。局部精氨酸(10− 3 mol/L,30分钟)不影响成年SHRSP对乙酰胆碱的反应,但增强老年SHRSP对乙酰胆碱(10− 5 mol/L)的血管舒张反应,而不影响硝普钠的反应。与此相反,d-精氨酸不影响乙酰胆碱诱导的血管舒张老年SHRSP。这些结果表明,受损的基底动脉扩张反应乙酰胆碱在老年SHRSP恢复到正常的byl-精氨酸,一氧化氮合酶的底物。
The objective of this study was to test the hypothesis that administration ofl-arginine, a substrate for nitric oxide synthase, restores acetylcholine-induced dilatation of the basilar artery in chronically hypertensive rats. Basilar artery diameter was measured through a cranial window in anesthetized stroke-prone spontaneously hypertensive rats (SHRSP) and normotensive Wistar-Kyoto rats (WKY) aged 6 to 7 months (adult) and 12 months (older adult). Under control conditions, baseline basilar artery diameter was smaller in SHRSP (adult, 239±30 μm; older adult, 198±13 μm) (mean±SE) than in WKY (adult, 261±10 μm; older adult, 259±7 μm) (P<.05 versus SHRSP). Topical application of acetylcholine (10−5mol/L) produced dilatation of the basilar artery in WKY, which was impaired in both adult and older SHRSP (P<.05). Topicall-arginine (10−3mol/L for 30 minutes) did not affect responses to acetylcholine in adult SHRSP but enhanced vasodilatation in response to acetylcholine (10−5mol/L) in older SHRSP without affecting responses to sodium nitroprusside. In contrast,d-arginine did not affect acetylcholine-induced vasodilatation in older SHRSP. These results suggest that impaired dilatation of the basilar artery in response to acetylcholine in older SHRSP is restored toward normal byl-arginine, a substrate for nitric oxide synthase.