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Titolo:
Functional and cellular interactions between nitric oxide and prostacyclin
Autore:
Marcelin-Jimenez, G; Escalante, B;
Indirizzi:
IPN, Ctr Invest & Estudios Avanzados, Dept Mol Biomed, Mexico City 07300, DF, Mexico IPN Mexico City DF Mexico 07300 Mol Biomed, Mexico City 07300, DF, Mexico IPN, Ctr Invest & Estudios Avanzados, Dept Pharmacol & Toxicol, Mexico City 07300, DF, Mexico IPN Mexico City DF Mexico 07300 & Toxicol, Mexico City 07300, DF, Mexico
Titolo Testata:
COMPARATIVE BIOCHEMISTRY AND PHYSIOLOGY C-TOXICOLOGY & PHARMACOLOGY
fascicolo: 4, volume: 129, anno: 2001,
pagine: 349 - 359
SICI:
1532-0456(200108)129:4<349:FACIBN>2.0.ZU;2-M
Fonte:
ISI
Lingua:
ENG
Soggetto:
AORTIC ENDOTHELIAL-CELLS; VASCULAR SMOOTH-MUSCLE; RELAXING FACTOR; SIMULTANEOUS GENERATION; PLATELET-AGGREGATION; CORONARY-ARTERIES; PULMONARY-ARTERY; SYNTHASE; PEROXYNITRITE; CYCLOOXYGENASE;
Keywords:
cyclooxygenase; isolated perfused heart; nitric oxide; nitrovasodilators; prostacyclin; arachidonic acid; endothelial cells; coronary circulation; guanylate cyclase;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
34
Recensione:
Indirizzi per estratti:
Indirizzo: Escalante, B IPN, Ctr Invest & Estudios Avanzados, Dept Mol Biomed, Ave Inst Politecn Nacl 2508, Mexico City 07300, DF, Mexico IPN Ave Inst Politecn Nacl 2508 Mexico City DF Mexico 07300 o
Citazione:
G. Marcelin-Jimenez e B. Escalante, "Functional and cellular interactions between nitric oxide and prostacyclin", COMP BIOC C, 129(4), 2001, pp. 349-359

Abstract

Nitric oxide (NO) and rostacyclin (PGI(2)) can be released by vascular agents to synergize e their effects on vascular relaxation. In the present study we assess whether NO could affect PGI(2) production. We evaluated the effect of NO on PGI(2)-Mediated arachidonic acid (AA)-induced relaxation in the perfused heart. We used cultured endothelial cells to characterize the mechanism involved in the NO effect on PGI2 synthesis. AA-induced PGI(2) synthesis was enhanced when NO synthesis was inhibited. NO inhibited AA-induced relaxation and PGI(2) release in the coronary circulation. S-Nitroso-acetyl-DL-penicillamine (SNAP) decreased PGI, production in cultured endothelial cells. The SNAP effect was blunted by the inhibitor of soluble guanylate cyclase (LY-83,583) and the blocker of cGMP-dependent protein kinases (H-9). Specific cyclooxygenase-1 (COX-1) immunoprecipitation was associated to co-precipitation of four proteins. COX-I showed neither serine nor threoninephosphorylation. One of the proteins that co-precipitated with COX-I presented increased serine phosphorylation in the presence of SNAP This effect was inhibited by the H-9. We suggest that NO, through cGMP-dependent proteinkinases, produces the phosphorylation of a 104-kDa protein that is associated with inhibition in the activity of the COX-1, decreasing PGI, synthesisand thereby decreasing coronary PGI(2)-mediated vasodilatation. (C) 2001 Elsevier Science Inc. All rights reserved.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 31/03/20 alle ore 04:31:08