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Titolo:
Increased contribution of L-arginine-nitric oxide pathway in aorta of micelacking the gene for vimentin
Autore:
Zhang, J; Henrion, D; Ebrahimian, T; Benessiano, J; Colucci-Guyon, E; Langa, F; Levy, BI; Boulanger, CM;
Indirizzi:
Hop Lariboisiere, INSERM, U541, F-75475 Paris 10, France Hop LariboisiereParis France 10 INSERM, U541, F-75475 Paris 10, France Inst Pasteur, CNRS, URA 1960, Paris, France Inst Pasteur Paris FranceInst Pasteur, CNRS, URA 1960, Paris, France
Titolo Testata:
JOURNAL OF CARDIOVASCULAR PHARMACOLOGY
fascicolo: 4, volume: 38, anno: 2001,
pagine: 552 - 560
SICI:
0160-2446(200110)38:4<552:ICOLOP>2.0.ZU;2-Z
Fonte:
ISI
Lingua:
ENG
Soggetto:
ENDOTHELIUM-DEPENDENT CONTRACTIONS; MESENTERIC RESISTANCE ARTERIES; SHEAR-STRESS; EXPRESSION; MEDIATION; CELLS; MECHANOTRANSDUCTION; CYTOSKELETON; RELEASE;
Keywords:
acetylcholine; endothelium-dependent relaxation; cyclic guanosine monophosphate; cyclooxygenase;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
28
Recensione:
Indirizzi per estratti:
Indirizzo: Boulanger, CM Hop Lariboisiere, INSERM, U541, 41 Blvd Chapelle, F-75475 Paris 10, France Hop Lariboisiere 41 Blvd Chapelle Paris France 10 0, France
Citazione:
J. Zhang et al., "Increased contribution of L-arginine-nitric oxide pathway in aorta of micelacking the gene for vimentin", J CARDIO PH, 38(4), 2001, pp. 552-560

Abstract

Experiments were designed to investigate endothelial function in the aortaof mice lacking the gene for the cytoskeleton protein vimentin (vim(-/-)). Rings with and without endothelium from wild-type (vim(+/+)), heterozygous(vim(+/-)), and homozygous (vim(-/-)) mice were suspended in organ chambers to record of changes in isometric tension. During phenylephrine contraction, acetylcholine evoked comparable endothelium-dependent relaxations in the three groups. In the presence of N-omega-nitro-L-arginine, acetylcholine caused endothelium-dependent contractions, which were greater in vim(-/-) than in vim(+/+) and vim(+/-) aortas. Indomethacin did not affect relaxationto acetylcholine in vim(+/+) or in vim(+/-), but it significantly increased the maximal response in vim(-/-) (67 +/- 7 vs. 102 +/- 4%). Response to acetylcholine in vim(-/-) aortas was not affected by cyclooxygenase type 2 inhibitor NS-398, the thromboxane receptor antagonist SQ-29,548, or superoxide dismutase. Relaxations to sodium nitroprusside were not different between vim(+/+) and vim-mice and were not affected by cyclooxygenase inhibition. Cyclic guanosine monophosphate levels, which were increased to a comparable level by acetylcholine in vim(+/+) and vim(-/-), were augmented by indomethacin in vim(-/-) aortas but not in vim(+/+) aortas. Expression of endothelial nitric oxide synthase was not different between vim(+/+) and vim(-/-) preparations. These results suggest that despite comparable endothelium-dependent responses to acetylcholine, endothelial cells from vim(-/-) mice release a cyclooxygenase product that compensates the augmented contribution of nitric oxide.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 04/12/20 alle ore 15:53:05