INTERLEUKIN-2 CAUSES ENDOTHELIUM-DEPENDENT CONTRACTIONS TO ARACHIDONIC-ACID
INTERLEUKIN-2 CAUSES ENDOTHELIUM-DEPENDENT CONTRACTIONS TO ARACHIDONIC-ACID
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DOI：
10.1161/01.hyp.21.3.289
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发表时间：
1993-03-01
期刊：
影响因子：
8.3
通讯作者：
VANHOUTTE, PM
中科院分区：
文献类型：
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作者：
BOULANGER, CM;VANHOUTTE, PM
本实验旨在研究白细胞介素2（IL-2）对花生四烯酸（AA）诱导的Wistar-Kyoto（WKY）和自发性高血压大鼠（SHR）血管环内皮损伤的影响。在对照环中，花生四烯酸诱导的WKY主动脉收缩在有内皮和无内皮的制剂之间没有差异。与白细胞介素-2（10单位/mL）孵育6或18小时，增强了对花生四烯酸的反应，在环，但不是在那些没有，从WKY大鼠血管内皮。在WKY主动脉中，吲哚美辛和ridogrel（一种血栓烷内过氧化物受体拮抗剂和血栓烷合酶抑制剂）消除了与白细胞介素-2孵育后观察到的对花生四烯酸的内皮依赖性和内皮非依赖性收缩，但不受达唑昔苯（一种血栓烷合酶抑制剂）的影响。白细胞介素-2没有增加WKY主动脉平滑肌对U46619激活血栓素-内过氧化物受体的血管反应性。在自发性高血压大鼠的动脉粥样硬化中，花生四烯酸引起内皮依赖性收缩;白细胞介素-2没有改变有和无内皮的制剂对花生四烯酸的反应。这些数据表明：1）在SHR中观察到对花生四烯酸的内皮依赖性收缩，但在WKY大鼠主动脉中未观察到; 2）白细胞介素-2诱导WKY主动脉中对花生四烯酸的内皮依赖性收缩，这是由环氧合酶代谢物的增加释放介导的，该代谢物不同于血栓烷A，但激活血栓烷内过氧化物受体;白细胞介素2不影响SHR主动脉对花生四烯酸的内皮依赖性和非内皮依赖性反应。
The present experiments were designed to investigate the effect of interleukin-2 on the response to arachidonic acid in rings with and without endothelium from Wistar-Kyoto (WKY) and spontaneously hypertensive rat (SHR) aortas. In control rings, arachidonic acid induced contractions of WKY aorta that were not different between preparations with and without endothelium. Incubation with interleukin-2 (10 units/mL) for 6 or 18 hours augmented the response to arachidonic acid in rings with, but not in those without, endothelium from WKY rat aortas. In the WKY aorta, both the endothelium-dependent and endothelium-independent contractions to arachidonic acid observed after incubation with interleukin-2 were abolished by indomethacin and ridogrel (a thromboxane-endoperoxide receptor antagonist and a thromboxane synthase inhibitor) but were not affected by dazoxiben (a thromboxane synthase inhibitor). Interleukin-2 did not augment the vascular reactivity of WKY aortic smooth muscle to activation of the thromboxane-endoperoxide receptor with U46619. In aortas from SHRs, arachidonic acid evoked endothelium-dependent contraction; interleukin-2 did not modify the response to arachidonic acid in preparations with and without endothelium. These data demonstrate that 1) endothelium-dependent contractions to arachidonic acid are observed in SHR but not in WKY rat aortas; 2) interleukin-2 induces endothelium-dependent contractions to arachidonic acid in the WKY aorta that are mediated by an augmented release of a metabolite of cyclooxygenase, different from thromboxane A, but activating thromboxane-endoperoxide receptors; and 3) interleukin-2 does not affect the endothelium-dependent and endothelium-independent response to arachidonic acid in the SHR aorta.