GOU-TENG (FROM UNCARIA-RHYNCHOPHYLLA MIQUEL)-INDUCED ENDOTHELIUM-DEPENDENT AND ENDOTHELIUM-INDEPENDENT RELAXATIONS IN THE ISOLATED RAT AORTA
GOU-TENG (FROM UNCARIA-RHYNCHOPHYLLA MIQUEL)-INDUCED ENDOTHELIUM-DEPENDENT AND ENDOTHELIUM-INDEPENDENT RELAXATIONS IN THE ISOLATED RAT AORTA
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DOI：
10.1016/0024-3205(94)00715-2
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发表时间：
1994-01-01
期刊：
影响因子：
6.1
通讯作者：
SUGA, T
中科院分区：
文献类型：
--
作者：
KURAMOCHI, T;CHU, J;SUGA, T
钩藤是一种中药，用于治疗高血压。其降压作用已在自发性高血压大鼠(SHR)中得到证实。本文对其血管舒缩作用及其作用机制进行了体外研究。狗藤提取物(GTE)对去甲肾上腺素(NE)预收缩的Wistar京都大鼠(WKY)主动脉环标本具有和不具有完整内皮的松弛作用，后者的敏感性明显低于前者。N-G-单甲基-L-精氨酸可剂量依赖性地抑制GTE诱导的内皮依赖性松弛，而消炎痛不影响这种松弛。阿托品可抑制乙酰胆碱(ACh)诱导的内皮依赖松弛，但不抑制GTE诱导的内皮依赖松弛。此外，一旦应用GTE，即使在反复洗涤后，NE引起的随后的收缩也显著减少。NMMA有效地减少了GTE的这种残留效应，甚至逆转了这种影响。上述结果表明，GTE通过内皮依赖性和非依赖性机制对NE预收缩的大鼠主动脉起到松弛作用。内皮依赖性成分可能是通过EDRF/NO途径介导的，而不涉及M胆碱能受体。因此，GTE似乎主要通过释放EDRF/NO而成为一种有效和持久的血管扩张剂。
Gou-teng is a drug used for treatment of hypertension in Chinese medicine. Its antihypertensive action has been previously confirmed in the spontaneously hypertensive rat (SHR). Here, its vasorelaxing effect and the mechanisms of actions were studied in vitro. Gou-teng extract (GTE) relaxed the norepinephrine (NE)-precontracted aortic ring preparations isolated from Wistar Kyoto rats (WKY) with and without intact endothelium; the latter was significantly less sensitive than the former. The GTE-induced endothelium-dependent relaxation was significantly inhibited by N-G-monomethyl-L-arginine (NMMA) in a dose-dependent manner while indomethacin did not affect the relaxation. Atropine inhibited the acetylcholine (ACh)-induced endothelium-dependent relaxation but did not the GTE-induced one. Furthermore, once GTE was applied, the following NE-induced contraction was significantly reduced even after repeated washout. NMMA effectively reduced and rather reversed this residual effect of GTE. From these results, it is concluded that GTE relaxes the NE-precontracted rat aorta through endothelium-dependent and, to lesser extent, -independent mechanisms. The endothelium-dependent component would be mediated by EDRF/NO pathway in which the muscarinic cholinoceptors were not involved. Thus, GTE appears to be a potent and long-lasting vasodilator mainly through EDRF/NO release.