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Titolo:
STUDY OF THE MECHANISMS INVOLVED IN ADENOSINE-5'-O-(2-THIODIPHOSPHATE) INDUCED RELAXATION OF RAT THORACIC AORTA AND PANCREATIC VASCULAR BED
Autore:
SAIAG B; HILLAIREBUYS D; CHAPAL J; PETIT P; PAPE D; RAUL B; ALLAIN H; LOUBATIERESMARIANI MM;
Indirizzi:
FAC PHARM MONTPELLIER,PHYSIOL LAB,UNITE BIOL PAROI VASC,2 RUE PROF BERNARD F-35043 RENNES FRANCE FAC PHARM MONTPELLIER,PHARMACOL LAB F-34060 MONTPELLIER 01 FRANCE FAC MED MONTPELLIER,PHARMACOL LAB F-35043 RENNES FRANCE
Titolo Testata:
British Journal of Pharmacology
fascicolo: 3, volume: 118, anno: 1996,
pagine: 804 - 810
SICI:
0007-1188(1996)118:3<804:SOTMII>2.0.ZU;2-I
Fonte:
ISI
Lingua:
ENG
Soggetto:
ARTERIAL SMOOTH-MUSCLE; ENDOTHELIAL-CELLS; NITRIC-OXIDE; RELAXING FACTOR; ADENOSINE-TRIPHOSPHATE; HYPERPOLARIZING FACTOR; PROSTACYCLIN RELEASE; P2 PURINOCEPTORS; PULMONARY-ARTERY; BLOOD-VESSELS;
Keywords:
ADP-BETA-S; P-2-PURINOCEPTORS; L-NAME; INDOMETHACIN; REACTIVE BLUE 2; VASODILATATION; RAT THORACIC AORTA; PANCREATIC VASCULAR BED;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Science Citation Index Expanded
Citazioni:
51
Recensione:
Indirizzi per estratti:
Citazione:
B. Saiag et al., "STUDY OF THE MECHANISMS INVOLVED IN ADENOSINE-5'-O-(2-THIODIPHOSPHATE) INDUCED RELAXATION OF RAT THORACIC AORTA AND PANCREATIC VASCULAR BED", British Journal of Pharmacology, 118(3), 1996, pp. 804-810

Abstract

1 The endothelium-dependent relaxation of blood vessels induced by P-2Y-purinoceptor activation has often been shown to involve prostacyclin and/or nitric oxide (NO) release. In this work, we have investigatedthe mechanisms involved in the relaxant effect of the P-2Y agonist, adenosine -5'-O-(2-thiodiphosphate) (ADP beta S) using two complementary preparations: rat pancreatic vascular bed and aortic ring. 2 On the pancreatic vascular bed, ADP beta S (1.5 and 15 mu M) infused for 30 min induced a concentration-dependent vasodilatation; it was progressive during the first 10 min (first period) and sustained from 10 to 30 min (second period). Indomerhacin (10 mu M) delayed ADP beta S-induced vasodilatation (1.5 and 15 mu M) by about 6 min. N-omega-nitro-L-arginine methyl ester (L-NAME) (200 mu M) suppressed the relaxation for about 5 min but thereafter-ADP beta S at the two concentrations progressively induced an increase in the flow rate. Even the co-administration of L-NAME and indomethacin did not abolish the ADP beta S-induced vasorelaxation. 3 On 5-hydroxy tryptamine (5-HT) precontracted rings mounted in isometric conditions in organ baths, we observed that ADP beta Sinduced a concentration-dependent relaxation of rings with a functional endothelium; this effect was stable for 25 min. The ADP beta S relaxant effect was strongly inhibited by Reactive Blue 2 (30 mu M) and was suppressed by pretreatment of rings with saponin (0.05 mg ml(-1) for30 min), which also abolished the acetylcholine-induced relaxation. 4ADP beta S-induced relaxation of 5-HT precontracted rings is largely inhibited by indomethacin (100 or 10 mu M) or L-NAME (100 mu M). 5 We conclude that: the ADP beta S-induced relaxation is endothelium-dependent, mediated by P-2Y-purinoceptors, and at least in part linked to NOand prostacyclin release, depending on the preparation used. Furthermore, on the pancreatic vascular bed, (an)other mechanism(s) than prostacyclin and NO releases may be involved in ADP beta S-induced vasodilatation.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 15/07/20 alle ore 08:26:53