Boulanger C M, Vanhoutte P M
Department of Medicine-Hypertension, Baylor College of Medicine, Houston, Tex. 77030.
Hypertension. 1993 Mar;21(3):289-93. doi: 10.1161/01.hyp.21.3.289.
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 A2 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.
本实验旨在研究白细胞介素-2对来自Wistar-Kyoto（WKY）大鼠和自发性高血压大鼠（SHR）主动脉、带有和不带有内皮的血管环中花生四烯酸反应的影响。在对照血管环中，花生四烯酸诱导WKY主动脉收缩，有内皮和无内皮的标本之间无差异。用白细胞介素-2（10单位/毫升）孵育6或18小时增强了来自WKY大鼠主动脉、有内皮但无内皮的血管环对花生四烯酸的反应。在WKY主动脉中，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非内皮依赖性收缩均被吲哚美辛和利托格雷（一种血栓素-内过氧化物受体拮抗剂和血栓素合酶抑制剂）消除，但不受达唑氧苯（一种血栓素合酶抑制剂）影响。白细胞介素-2未增强WKY主动脉平滑肌对用U46619激活血栓素-内过氧化物受体的血管反应性。在SHR的主动脉中，花生四烯酸引起内皮依赖性收缩；白细胞介素-2未改变有内皮和无内皮标本中对花生四烯酸的反应。这些数据表明：1）在SHR的主动脉中观察到对花生四烯酸的内皮依赖性收缩，而在WKY大鼠主动脉中未观察到；2）白细胞介素-2在WKY主动脉中诱导对花生四烯酸的内皮依赖性收缩，其由环氧化酶代谢产物的释放增加介导，该代谢产物不同于血栓素A2但可激活血栓素-内过氧化物受体；3）白细胞介素-2不影响SHR主动脉中对花生四烯酸的内皮依赖性和非内皮依赖性反应。
