Park S J, Lee J J, Vanhoutte P M
Center for Experimental Therapeutics, Department of Medicine, Baylor College of Medicine, One Baylor Plaza, Houston, TX 77030, USA.
Zhongguo Yao Li Xue Bao. 1999 Oct;20(10):872-8.
To determine the role of endothelium-derived contracting factor (EDCF) in the response to endothelin-1 in arteries with regenerated endothelium.
Rings of porcine coronary arteries, with and without endothelium of previously deendothelialized left anterior descending coronary arteries and native left circumflex coronary arteries, were suspended in conventional organ chambers for the measurement of isometric force.
In quiescent rings of the previously deendothelialized left anterior descending coronary artery treated with the NO-synthase inhibitor nitro-L-arginine, endothelin-1 caused contractions which were larger in rings with than that in those without endothelium. Under the same experimental conditions, in the left circumflex coronary artery, the contractions to endothelin-1 were augmented markedly by the removal of the endothelium. In rings with endothelium of the previously deendothelialized left anterior descending coronary artery, indometacin (inhibitor of cyclooxygenase) and ridogrel (thromboxane A2 receptor antagonist and inhibitor of thromboxane synthase) inhibited contractions to endothelin-1. Dazoxiben (inhibitor of thromboxane synthase) inhibited, to the same extent as indometacin and ridogel, the response to higher concentrations of endothelin-1. The endothelium-dependent component of the response to lower concentrations of endothelin-1 was inhibited by indometacin and ridogrel, but not by dazoxiben. In rings without endothelium of both previously deendothelialized left anterior descending and native left circumflex coronary arteries, indometacin and ridogrel did not affect the contractions to endothelin-1.
These findings suggest that in regenerated endothelium, high concentrations of endothelin-1 stimulate the release of thromboxane A2. Endoperoxides generated by activation of endothelial cyclooxygenase may be the endothelium-derived contracting factor(s) released in regenerated endothelium by lower concentrations of the peptide.
确定内皮衍生收缩因子（EDCF）在再生内皮动脉对内皮素-1反应中的作用。
将猪冠状动脉环，包括先前去内皮的左前降支冠状动脉和天然左旋支冠状动脉有内皮和无内皮的环，悬挂在传统器官浴槽中测量等长力。
在用一氧化氮合酶抑制剂硝基-L-精氨酸处理的先前去内皮的左前降支冠状动脉的静息环中，内皮素-1引起的收缩在有内皮的环中比无内皮的环中更大。在相同实验条件下，在左旋支冠状动脉中，去除内皮后对内皮素-1的收缩明显增强。在先前去内皮的左前降支冠状动脉有内皮的环中，吲哚美辛（环氧化酶抑制剂）和利多格雷（血栓素A2受体拮抗剂和血栓素合酶抑制剂）抑制对内皮素-1的收缩。达唑氧苯（血栓素合酶抑制剂）与吲哚美辛和利多格雷一样，抑制对较高浓度内皮素-1的反应。吲哚美辛和利多格雷抑制对较低浓度内皮素-1反应的内皮依赖性成分，但达唑氧苯无此作用。在先前去内皮的左前降支冠状动脉和天然左旋支冠状动脉无内皮的环中，吲哚美辛和利多格雷不影响对内皮素-1的收缩。
这些发现表明，在再生内皮中，高浓度的内皮素-1刺激血栓素A2的释放。内皮环氧化酶激活产生的内过氧化物可能是该肽较低浓度时在再生内皮中释放的内皮衍生收缩因子。
