Catalogo Articoli (Spogli Riviste)

OPAC HELP

Titolo:
CA-VALVE(+ MOBILIZATION MEDIATED BY ENDOTHELIN ET(A) RECEPTOR IN ENDOTHELIUM OF RABBIT AORTIC)
Autore:
AMANO K; HORI M; OZAKI H; MATSUDA Y; KARAKI H;
Indirizzi:
UNIV TOKYO,FAC AGR,DEPT VET PHARMACOL,BUNKYO KU,YAYOI 1-1-1 TOKYO 113JAPAN UNIV TOKYO,FAC AGR,DEPT VET PHARMACOL,BUNKYO KU TOKYO 113 JAPAN KYOWA HAKKO KYOGO CO,TOKYO RES LABS TOKYO JAPAN
Titolo Testata:
The Journal of pharmacology and experimental therapeutics
fascicolo: 3, volume: 271, anno: 1994,
pagine: 1359 - 1364
SICI:
0022-3565(1994)271:3<1359:CMMBEE>2.0.ZU;2-J
Fonte:
ISI
Lingua:
ENG
Soggetto:
SMOOTH-MUSCLE; NITRIC-OXIDE; SELECTIVE AGONIST; B RECEPTOR; RAT AORTA; CELLS; IRL-1620; CALCIUM; SUBTYPE; PROSTACYCLIN;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
29
Recensione:
Indirizzi per estratti:
Citazione:
K. Amano et al., "CA-VALVE(+ MOBILIZATION MEDIATED BY ENDOTHELIN ET(A) RECEPTOR IN ENDOTHELIUM OF RABBIT AORTIC)", The Journal of pharmacology and experimental therapeutics, 271(3), 1994, pp. 1359-1364

Abstract

The mechanism of Ca++ mobilization induced by endothelins (ETs) and the receptor subtype responsible for this effect were examined in the endothelium of rabbit aortic valve. In the endothelium loaded with fura-2, ET-1 (1-100 nM) induced large transient increase followed by smallsustained increase in cytosolic Ca++ level ([Ca++](i)) in a concentration-dependent manner. ET-3 induced only a small increase in [Ca++](i)at higher concentrations (100-300 nM) than ET-1, whereas a selective ET(B) agonist, 100 nM IRL 1620 (succinyl-[Glu(9), Ala(11,15)]ET-1 (8-21)), was ineffective. A selective ET(A) antagonist, 3 mu M BQ-123, (cyclo [-Asp-Pro-Val-Leu-Trp-]) but not a selective ET(B) antagonist, 10 mu M RES-701-1 [cyclic (Gly(1)-Asp(9)) -Gly-Thr-Ala-Pro-Asp-Trp-Phe-Phe-Asn-Tyr-Tyr-Trp)] inhibited the effects of ET-1 and ET-3. The sustained increase in [Ca++](i) induced by ET-1 was abolished by 30 mu M La++, although 100 nM nicardipine was ineffective. In the absence of external Ca++ (with 0.5 mM EGTA), ET-1 induced only a transient increase in [Ca++](i), which was inhibited by an inhibitor of Ca++-ATPase in endoplasmic reticulum, 1 mu M thapsigargin. However, an inhibitor and anactivator of Ca++-induced Ca++-release channel, 10 mu M ryanodine and10 mM caffeine, did not change [Ca++](i). These results suggest that,in the endothelium of rabbit aortic valve, only the ET(A) receptor mediates the effects of ETs to increase [Ca++](i) which is attributable to the release of Ca++ from thapsigargin-sensitive and ryanodine-insensitive Ca++ stores and also to the Ca++ influx through La+++-sensitiveand dihydropyridine-insensitive Ca++ channels.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 03/07/20 alle ore 22:02:51