AGGREGATION OF HUMAN POLYMORPHONUCLEAR LEUKOCYTES BY ENDOTHELIN - ROLE OF PLATELET-ACTIVATING-FACTOR

被引：67

作者：

GOMEZGARRE, D ^{[1
]}

GUERRA, M ^{[1
]}

GONZALEZ, E ^{[1
]}

LOPEZFARRE, A ^{[1
]}

RIESCO, A ^{[1
]}

CARAMELO, C ^{[1
]}

ESCANERO, J ^{[1
]}

EGIDO, J ^{[1
]}

机构：

[1] UNIV AUTONOMA MADRID, FDN JIMENEZ DIAZ, NEFROL LAB, AVE REYES CATOLICOS S, E-28040 MADRID, SPAIN

来源：

EUROPEAN JOURNAL OF PHARMACOLOGY | 1992年 / 224卷 / 2-3期

关键词：

ENDOTHELIN; AGGREGATION; POLYMORPHONUCLEAR LEUKOCYTES; PAF(PLATELET-ACTIVATING FACTOR; PAF-ACETHER);

D O I：

10.1016/0014-2999(92)90801-A

中图分类号：

R9 [药学];

学科分类号：

1007 ;

摘要：

The mechanisms by which endothelin-I (ET-1) acts on polymorphonuclear leukocytes (PMN) are insufficiently known. In this study, we assessed the hypotheses that ET-1 is a PMN-aggregating agent, and that platelet-activating factor (PAF) is the principal mediator of ET-1-induced PMN aggregation. ET-1 induced dose-related PMN aggregation, which started 1 min after ET-1 exposure. Two different specific PAF receptor antagonists blocked the effect of ET-1 on PMN aggregation. In addition, ET-1 induced a significant increase in the production of PAF by PMN after 2 to 5 min of ET-1 incubation. ET-1 induced PAF release from PMN rather than accumulation. This PAF production was dependent on intra- and extracellular Ca2+. In this regard, the PAF receptor antagonists significantly blunted the ET-1-induced peak in cytosolic free Ca2+([Ca2+]i). Our results, therefore, indicate that ET-1 is effective in causing aggregation of human PMN and that its action appears to be mediated by PAF production via a Ca2+-dependent mechanism.

引用

页码：167 / 172

页数：6

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