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Titolo:
ACTIONS OF 4-CHLORO-3-ETHYL PHENOL ON INTERNAL CA2-MUSCLE AND ENDOTHELIAL-CELLS( STORES IN VASCULAR SMOOTH)
Autore:
LOW AM; SORMAZ L; KWAN CY; DANIEL EE;
Indirizzi:
MCMASTER UNIV,DEPT BIOMED SCI,ROOM 4N47 HAMILTON ON L8N 3Z5 CANADA MCMASTER UNIV,DEPT BIOMED SCI HAMILTON ON L8N 3Z5 CANADA
Titolo Testata:
British Journal of Pharmacology
fascicolo: 3, volume: 122, anno: 1997,
pagine: 504 - 510
SICI:
0007-1188(1997)122:3<504:AO4POI>2.0.ZU;2-E
Fonte:
ISI
Lingua:
ENG
Soggetto:
SARCOPLASMIC-RETICULUM; CYCLOPIAZONIC ACID; GUINEA-PIG; INTRACELLULAR CA2+; CALCIUM SPARKS; INHIBITOR; RYANODINE; THAPSIGARGIN; CONTRACTION; RELAXATION;
Keywords:
4-CHLORO-3-ETHYL PHENOL; CA2+ IMAGING; DOG MESENTERIC ARTERY; BOVINE PULMONARY ARTERY ENDOTHELIAL CELLS; SARCOPLASMIC RETICULUM; RYANODINE; CA2+ RELEASE CHANNELS;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Science Citation Index Expanded
Citazioni:
24
Recensione:
Indirizzi per estratti:
Citazione:
A.M. Low et al., "ACTIONS OF 4-CHLORO-3-ETHYL PHENOL ON INTERNAL CA2-MUSCLE AND ENDOTHELIAL-CELLS( STORES IN VASCULAR SMOOTH)", British Journal of Pharmacology, 122(3), 1997, pp. 504-510

Abstract

1 Recently, 4-chloro-3-ethyl phenol (CEP) has been shown to cause therelease of internally stored Ca2+, apparently through ryanodine-sensitive Ca2+ channels, in fractionated skeletal muscle terminal cisternaeand in a variety of non-excitable cell types. Its action on smooth muscle is unknown. In this study, we characterized the actions of CEP onvascular contraction in endothelium-denuded dog mesenteric artery. Wealso determined its ability to release Ca2+, by use of Ca2+ imaging techniques, on dog isolated mesenteric artery smooth muscle cells and on bovine cultured pulmonary artery endothelial cells. 2 After phenylephrine-(PE, 10 mu M) sensitive Ca2+ stores were depleted by maximal PE stimulation in Ca2+-free medium, the action of CEP on refilling of theemptied PE stores was tested, by first preincubating the endothelium-denuded artery in CEP for 15 min before Ca2+ was restored for a 30 minrefilling period. At the end of this period, Ca2+ and CEP were removed, and the arterial ring was tested again with PE to assess the degreeof refilling of the internal Ca2+-store. 3 In a concentration-dependent manner (30, 100 and 300 mu M), CEP significantly reduced the size of the post-refilling PE contraction (49.4, 28.9 and 5.7% of control, respectively) in Ca2+-free media. This suggests that Ca2+ levels are reduced in the internal stores by CEP treatment. CEP alone did not causeany contraction either in Ca2+-containing or Ca2+-free Krebs solution. 4 Restoring Ca2+ in the presence of PE caused a large contraction, which reflects PE-induced influx of extracellular Ca2+. The contractionof tissues pretreated with 300 mu M CEP was significantly less compared with controls. However, tissues pretreated with 30 and 100 mu M CEPwere unaffected.. Washout of CEP over 30 min produced complete recovery of responses to PE in Ca2+-free and Ca2+-containing medium suggesting a rapid reversal of CEP effects. 5 Concentration-response curves were constructed for PE, 5-hydroxytryptamine (5-HT) and K+ in the absence of and after 30 min pre-incubation with 30, 100 and 300 mu M CEP. Inall cases, CEP caused a concentration-dependent depression of the maximum response to PE (84.8, 43.3 and 11.6% of control), 5-HT (65.4, 25.7 and 6.9% of control) and K+ (77.6, 41.1 and 10.8% of control). 6 Some arterial rings were pre-incubated with ryanodine (30 mu M) for 30 min before the construction of PE concentration-response curves. In Ca2+-free Krebs solution, ryanodine alone did not cause any contraction. However, 58% (11 out of 19) of the tissues tested with ryanodine developed contraction (6.9 +/- 1.2% of 100 mM K+ contraction, n = 11) in thepresence of external Ca2+. EC50 values for PE in ryanodine-treated tissues (1.7 +/- 0.25 mu M, n = 16) were not significantly different from controls (2.5 +/- 0.41 mu M, n = 22). Maximum contractions to PE (118.5 +/- 4.4% of 100 mM K+ contraction, n = 16) were also unaffected byryanodine when compared to controls (129 +/- 4.2%, n = 23). 7 When fura-2 loaded smooth muscle cells (n = 13) and endothelial cells (n = 27) were imaged for Ca2+ distribution, it was observed that 100 and 300 mu M CEP in Ca2+-free medium caused Ca2+ release in both cell types. Smooth muscle cells showed a small decrease in cell length. Addition ofEGTA (5 mM) reversed the effect of CEP on intracellular Ca2+ to control values. 8 These data show. for the first time in vascular smooth muscle and endothelial cells, that CEP releases Ca2+ more rapidly than ryanodine. Unlike ryanodine, CEP caused no basal contraction but depressed contractions to PE, 5-HT and K+. The lack of basal contraction mayresult from altered responsiveness of the contractile system to intracellular Ca2+ elevation.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 09/07/20 alle ore 18:06:48