INHIBITION BY L-ARGININE OF THE ENDOTHELIN-MEDIATED INCREASE IN CYTOSOLIC CALCIUM IN HUMAN NEUTROPHILS

被引：44

作者：

FARRE, AL ^{[1
]}

RIESCO, A ^{[1
]}

MOLIZ, M ^{[1
]}

EGIDO, J ^{[1
]}

CASADO, S ^{[1
]}

HERNANDO, L ^{[1
]}

CARAMELO, C ^{[1
]}

机构：

[1] FDN JIMENEZ DIAZ,NEFROL LAB,E-28040 MADRID,SPAIN

来源：

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS | 1991年 / 178卷 / 03期

关键词：

D O I：

10.1016/0006-291X(91)90974-C

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

The effect of endothelin (ET) on the cytosolic-free calcium ([Ca2+]i) changes in polymorphonuclear leukocytes (PMN) from normal humans and Wistar rats was investigated. ET induced a dose-related [Ca2+]i peak. This [Ca2+]i transient was blunted by TMB-8 (10-5M) and by Ca2+-free EGTA medium, therefore suggesting a role of both intracellular Ca2+ release and Ca2+ influx in the generation of the [Ca2+]i peak. Preincubation of PMN with the nitric oxide (NO)-donor L-arginine (L-Arg) markedly blocked the ET-induced [Ca2+]i transient in an enantiomerically-specific manner. A similar blunting effect of L-Arg on the fMLP (10-7M)-induced [Ca2+]i transient was detected. The L-Arg antagonist, NG-monomethyl-L-arginine (L-NMMA), reverted the L-Arg blocking effect on both ET- and fMLP-induced [Ca2+]i transients. These data suggest that ET has a potential role in activating Ca2+ mobilization in PMN, an effect that can be inhibited by L-Arg. © 1991.

引用

页码：884 / 891

页数：8

共 20 条

[1] STUDIES ON MECHANISM OF ACTION OF A NEW CA2+ ANTAGONIST, 8-(N,N-DIETHYLAMINO)OCTYL 3,4,5-TRIMETHOXYBENZOATE HYDROCHLORIDE IN SMOOTH AND SKELETAL-MUSCLES [J].