NITRIC-OXIDE INACTIVATES ENDOTHELIUM-DERIVED CONTRACTING FACTOR IN THE RAT AORTA
NITRIC-OXIDE INACTIVATES ENDOTHELIUM-DERIVED CONTRACTING FACTOR IN THE RAT AORTA
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DOI：
10.1161/01.hyp.19.5.442
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发表时间：
1992-05-01
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：
AUCHSCHWELK, W;KATUSIC, ZS;VANHOUTTE, PM
乙酰胆碱引起自发性高血压大鼠主动脉内皮源性舒张因子和收缩因子的同时释放。在正常血压控制下，只有放松因子在主动脉中释放。实验旨在确定内皮依赖性松弛抑制剂是否会改变内皮依赖性收缩。将有内皮和无内皮的正常和自发性高血压大鼠的胸主动脉环悬吊在器官室中进行等长张力记录。氧合血红蛋白（一种内皮源性松弛因子的清道夫）和N(G)-单甲基l -精氨酸（一种一氧化氮形成的抑制剂）增强了对乙酰胆碱的收缩。亚甲基蓝（一种可溶性鸟苷酸环化酶抑制剂）和超氧化物歧化酶（一种超氧化物阴离子清除剂）没有改变这些收缩。在氧合血红蛋白或N(G)-单甲基l -精氨酸存在时的收缩，与未处理的环一样，是内皮依赖性的；它们只出现在自发性高血压大鼠的主动脉中，并被吲哚美辛消除。在氧合血红蛋白存在的情况下，乙酰胆碱的收缩不受超氧化物歧化酶或去铁胺的影响。这些数据表明，内皮源性松弛因子抑制自发性高血压大鼠主动脉内皮依赖的乙酰胆碱收缩，可能是通过内皮源性收缩因子的化学失活，而不是通过刺激鸟苷酸环化酶或清除氧源性自由基。
Acetylcholine evokes the simultaneous release of endothelium-derived relaxing and contracting factors in aortas from spontaneously hypertensive rats. Only relaxing factors are released in aortas from normotensive controls. Experiments were designed to determine whether inhibitors of endothelium-dependent relaxations modify endothelium-dependent contractions. Rings of thoracic aortas of normotensive and spontaneously hypertensive rats, with and without endothelium, were suspended in organ chambers for isometric tension recording. Oxyhemoglobin (a scavenger of endothelium-derived relaxing factor) and N(G)-monomethyl L-arginine (an inhibitor of nitric oxide formation) augmented the contractions to acetylcholine. Methylene blue (an inhibitor of soluble guanylate cyclase) and superoxide dismutase (a scavenger of superoxide anions) did not modify these contractions. The contractions in the presence of oxyhemoglobin or N(G)-monomethyl L-arginine, like those in untreated rings, were endothelium-dependent; they only occurred in aortas from spontaneously hypertensive rats and were abolished by indomethacin. The contractions to acetylcholine in the presence of oxyhemoglobin were not affected by superoxide dismutase or deferoxamine. These data suggest that endothelium-derived relaxing factor inhibits endothelium-dependent contractions to acetylcholine in the spontaneously hypertensive rat aorta, probably by chemical inactivation of the endothelium-derived contracting factor rather than by stimulation of guanylate cyclase or scavenging of oxygen-derived free radicals.