CHEMOTACTIC PEPTIDE FMLP CONTRACTS HUMAN CORONARY-ARTERIES VIA CYCLOOXYGENASE PRODUCTS
CHEMOTACTIC PEPTIDE FMLP CONTRACTS HUMAN CORONARY-ARTERIES VIA CYCLOOXYGENASE PRODUCTS
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DOI：
10.1152/ajpheart.1990.258.3.h848
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发表时间：
1990-03-01
影响因子：
--
通讯作者：
FORSTERMANN, U
中科院分区：
文献类型：
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作者：
BODE, SM;KUHN, M;FORSTERMANN, U
趋化肽N-甲酰-L-甲硫氨酰-L-亮氨酰-L-苯丙氨酸（FMLP）是支气管平滑肌的收缩剂。最近，它也被证明通过一种未知的机制收缩兔冠状动脉。这促使我们研究趋化肽是否对心脏移植过程中获得的人冠状动脉张力有影响。FMLP对人冠状动脉条有强而有效的肌生长作用。收缩通常是短暂的，并受到快速耐受。FMLP诱导的血管收缩不依赖于内皮细胞的存在。反应不受组胺H1-拮抗剂苯海拉明或肽-白三烯FPL 55712的拮抗剂。然而，在脂肪酸环氧合酶抑制剂阿司匹林或吲哚美辛的存在下，收缩被完全消除。用FMLP刺激人冠状动脉环导致前列腺素（PG）F2 α的显著产生，PGD 2的产生较少，血栓素B2略有增加。所有这些前列腺素类使动脉收缩，但稳定的血栓烷模拟物U44069比PGF 2 α强100倍。或PGD 2。这些数据表明，FMLP激活人冠状动脉外膜或中膜中身份不明的细胞，产生血管收缩剂环氧合酶产物的混合物。这些化合物可能介导FMLP对该动脉的肌营养作用。该机制可能参与了某些形式的冠状动脉血管痉挛的发病机制。
The chemotactic peptide N-formyl-L-methionyl-L-leucyl-L-phenylalanine (FMLP) is a constrictor of bronchial smooth muscle. Recently it has also been shown to contract rabbit coronary arteries by an unknown mechanism. This prompted us to investigate whether the chemotactic peptide has an effect on the tone of human coronary arteries obtained during heart transplantation. FMLP was found to be a potent and efficacious myotropic agent on strips of human coronary artery. Contractions were generally transient and subject to tachyphylaxis. The FMLP-induced vasoconstriction was not dependent on the presence of endothelial cells. The response was unaffected by the histamine H1-antagonist diphenyhydramine or the antagonist of peptido-leukotrienes FPL 55712. However, the contraction were completely abolished in the presence of the fatty acid cyclooxygenase inhibitors aspirin or indomethacin. Stimulation of rings of human coronary artery with FMLP resulted in a marked production of prostaglandin (PG)F2.alpha., a smaller production of PGD2, and a slight increase in thromboxane B2. All these prostanoids constricted the artery, but the stable thromboxane mimetic U44069 was 100 times more potent than PGF2.alpha. or PGD2. These data indicate that FMLP activates cells of unknown identity in the adventitia or media of human coronary arteries to produce a mixture of vasoconstrictor cyclooxygenase products. These compounds are likely to mediate the myotropic effect of FMLP on this artery. The mechanism may participate in the pathogenesis of some forms of coronary vasospasm.