VASCULAR SMOOTH-MUSCLE RELAXATION INDUCED BY EPIDERMAL GROWTH-FACTOR IS ENDOTHELIUM-DEPENDENT
VASCULAR SMOOTH-MUSCLE RELAXATION INDUCED BY EPIDERMAL GROWTH-FACTOR IS ENDOTHELIUM-DEPENDENT
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DOI：
10.1016/0014-2999(90)90308-s
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发表时间：
1990-05-16
影响因子：
5
通讯作者：
AKATSUKA, N
中科院分区：
文献类型：
--
作者：
NAMIKI, A;AKATSUKA, N
表皮生长因子（EGF）是血小板在聚集过程中释放出来的。因为我们认为EGF在血管张力中起作用，我们使用有和没有内皮的离体大鼠主动脉条研究其血管反应性。在内皮存在下，EGF松弛用40 mM K+、10-5 M前列腺素F2 α预收缩的血管平滑肌。或10-6 M去甲肾上腺素。EGF诱导的松弛作用在前列腺素F2 α上更为显著。和去甲肾上腺素引起的收缩比K+引起的收缩。阿托品（10 ~（-5）M）和阿司匹林（10 ~（-5）M）对EGF引起的血管舒张无影响，而亚甲蓝（10 ~（-5）M）可部分阻断EGF引起的血管舒张。这些结果表明，EGF松弛血管平滑肌的内皮细胞的存在。他们还表明，表皮生长因子对内皮细胞产生不依赖于环氧合酶的松弛因子的影响;释放因子激活可溶性鸟苷酸环化酶，通过产生环GMP导致血管平滑肌松弛。
Epidermal growth factor (EGF) is released from platelets during aggregation. Because we thought that EGF played a role in vascular tone, we investigated its vascular reactivity using isolated rat aortic strips with and without the endothelium. In the presence of endothelium, EGF relaxed vascular smooth muscle precontracted with 40 mM K+, 10-5 M prostaglandin F2.alpha. or 10-6 M norepinephrine. The relaxation induced by EGF was more prominent on the prostaglandin F2.alpha.- and norepinephrine-induced contractions than on the K+-induced contraction. Atropine (10-5 M) and aspirin (10-5 M) had no effect on the EGF-induced relaxation, but methylene blue (10-5 M) partly abolished the relaxation evoked by EGF. These results suggest that EGF relaxes vascular smooth muscle in the presence of the endothelium. They also suggest that EGF has an effect on the endothelium to produce relaxing factor independent of cyclooxygenase; the releasing factor activates soluble guanylate cyclase, resulting in relaxation of vascular smooth muscle through the production of cyclic GMP.