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Titolo:
SELECTIVE-INHIBITION BY BARBITURATES OF THE SYNTHESIS OF ENDOTHELIUM-DERIVED HYPERPOLARIZING FACTOR IN THE RABBIT CAROTID-ARTERY
Autore:
LISCHKE V; BUSSE R; HECKER M;
Indirizzi:
JOHANN WOLFGANG GOETHE UNIV CLIN,CTR PHYSIOL,THEODAR STERN KAI 7 D-60590 FRANKFURT GERMANY JOHANN WOLFGANG GOETHE UNIV CLIN,CTR PHYSIOL D-60590 FRANKFURT GERMANY JOHANN WOLFGANG GOETHE UNIV CLIN,DEPT ANAESTHESIOL D-60590 FRANKFURT GERMANY
Titolo Testata:
British Journal of Pharmacology
fascicolo: 6, volume: 115, anno: 1995,
pagine: 969 - 974
SICI:
0007-1188(1995)115:6<969:SBBOTS>2.0.ZU;2-5
Fonte:
ISI
Lingua:
ENG
Soggetto:
ARACHIDONIC-ACID; CORONARY-ARTERIES; SKELETAL-MUSCLE; K+ CHANNELS; RAT; BRADYKININ; ATTENUATE;
Keywords:
ENDOTHELIUM-DERIVED HYPERPOLARIZING FACTOR; NITRIC OXIDE; ACETYLCHOLINE; BARBITURATES; CAROTID ARTERY; CYTOCHROME P450;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
23
Recensione:
Indirizzi per estratti:
Citazione:
V. Lischke et al., "SELECTIVE-INHIBITION BY BARBITURATES OF THE SYNTHESIS OF ENDOTHELIUM-DERIVED HYPERPOLARIZING FACTOR IN THE RABBIT CAROTID-ARTERY", British Journal of Pharmacology, 115(6), 1995, pp. 969-974

Abstract

1 Several lines of evidence suggest that both volatile and intravenous anaesthetics may interfere with the synthesis and release of endothelium-derived vasoactive factors. We have investigated the effects of three different barbiturates on the release of nitric oxide (NO) and endothelium-derived hyperpolarizing factor (EDHF) in phenylephrine (1 muM)-preconstricted, endothelium-intact ring segments of the rabbit carotid artery. The segments were pretreated with the cyclo-oxygenase inhibitor, diclofenac (1 mu M), to prevent the formation of vasoactive prostanoids, such as prostacyclin (PGI(2)). 2 Acetylcholine (ACh) elicited a concentration-dependent relaxation (EC(50) 0.15 mu M) in control segments which was not significantly different from the relaxant responses of segments pretreated with methohexitone (0.03-0.3 mM), phenobarbitone (0.1-0.3 mM) or thiopentone (0.1-0.3 mM). 3 Inhibition of NO synthesis with N-G-nitro-L-arginine (O.1 mM) significantly reduced the maximum relaxant response to ACh from 96 to 40%. This NO/PGI(2)-independent relaxation appeared to be mediated by the release of EDHF, since it was strongly diminished in the presence of the K-ca(+) inhibitors, tetrabutylammonium (1-3 mM) and charybdotoxin (10 nM), following preconstriction with potassium calcium (40 mM) or removal of the endothelium. Thiopentone or methohexitone markedly attenuated the EDHF-mediated relaxant response to ACh, while phenobarbitone had no effect. The endothelium-independent relaxation elicited by sodium nitroprusside (0.01-10 mu M), on the other hand, was only marginally affected by these anaesthetics. 4 The cytochrome P450 inhibitor, clotrimazole (3-100 mu M),mimicked the inhibitory effect of thiopentone and methohexitone on the NO/PGI(2)-independent relaxant response to ACh. Moreover the cytochrome P450-catalyzed O-dealkylation of 7-ethoxycoumarin by rabbit liver microsomes was inhibited in the presence of thiopentone or methohexitone (0.3-1 mM), while phenobarbitone was without effect. 5 These findings suggest that thiopentone and methohexitone selectively attenuate the EDHF-mediated relaxant response to ACh in the rabbit carotid artery,presumably by interfering with its synthesis from arachidonic acid via the cytochrome P450 epoxygenase pathway.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 18/09/20 alle ore 19:15:03