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Titolo:
EFFECTS OF HOMOCYSTEINE ON ACETYLCHOLINE-INDUCED AND ADENOSINE-INDUCED VASODILATATION OF PANCREATIC VASCULAR BED IN RATS
Autore:
QUERE I; HILLAIREBUYS D; BRUNSCHWIG C; CHAPAL J; JANBON C; BLAYAC JP; PETIT P; LOUBATIERESMARIANI MM;
Indirizzi:
FAC MED MONTPELLIER,INST BIOL,PHARMACOL LAB,UPRES EA 1677,BLVD HENRI 4 F-34060 MONTPELLIER 01 FRANCE FAC MED MONTPELLIER,INST BIOL,PHARMACOL LAB,UPRES EA 1677 F-34060 MONTPELLIER 01 FRANCE HOP ST ELOI,SERV MED INTERNE MONTPELLIER FRANCE
Titolo Testata:
British Journal of Pharmacology
fascicolo: 2, volume: 122, anno: 1997,
pagine: 351 - 357
SICI:
0007-1188(1997)122:2<351:EOHOAA>2.0.ZU;2-T
Fonte:
ISI
Lingua:
ENG
Soggetto:
INDEPENDENT RISK FACTOR; MESENTERIC ARTERIAL BED; ENDOTHELIAL-CELL INJURY; SMOOTH-MUSCLE CELLS; HYPERPOLARIZING FACTOR; PLASMA HOMOCYSTEINE; CORONARY-ARTERY; NITRIC-OXIDE; ARTERIOSCLEROSIS; HYPERHOMOCYSTEINEMIA;
Keywords:
HOMOCYSTEINE; THIOL; VASODILATATION; ACETYLCHOLINE; ADENOSINE; PANCREATIC VASCULAR BED; ENDOTHELIAL CELLS;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Science Citation Index Expanded
Citazioni:
62
Recensione:
Indirizzi per estratti:
Citazione:
I. Quere et al., "EFFECTS OF HOMOCYSTEINE ON ACETYLCHOLINE-INDUCED AND ADENOSINE-INDUCED VASODILATATION OF PANCREATIC VASCULAR BED IN RATS", British Journal of Pharmacology, 122(2), 1997, pp. 351-357

Abstract

1 Epidemiological and experimental data have shown that homocysteine may provoke vascular lesions and that moderate homocysteinaemia may constitute an independent risk factor for vascular disease. It is now documented that homocysteine damages human endothelial cells in culture,possibly by producing hydrogen peroxide in an oxygen-dependent reaction. 2 In this study, we have examined the direct effect of this sulphur amino acid on pancreatic vascular resistance. Experiments were performed on the vascular bed of the rat isolated pancreas perfused al constant pressure; thus, any change in pancreatic vascular resistance resulted in a change in the flow rate. D,L-Homocysteine perfused for one hour at three different concentrations (200 mu M, 2 mM, 20 mM) did not induce any significant change in the flow rate per se. Homocysteine infusion for 30 min at a concentration of 200 mu M or 2 mM abolished theendothelium-dependent vasodilatation induced by acetylcholine (0.05 mu M), but did not modify adenosine (1.5 mu M)-induced vasodilatation. 3 The effect of D,L-homocysteine (200 mu M or 2 mM) cannot be ascribedto a direct antimuscarinic effect since 30 min pretreatment of rat ileum with these concentrations did not significantly change the contractile effect of increasing concentrations of acetylcholine (0.015-15 muM). 4 Preincubation of human umbilical vein endothelial cells with D,L-homocysteine (0.2-5.0 mM) had no significant effect on overall cell number or viability during 18 h of incubation; the endothelial cells exposed to concentrations up to 5 mM exhibited a spindle-shaped, whirled pattern. This pattern was reversed 48 h after the removal of homocysteine. A cytotoxic effect was seen after 18 h incubation in 10 mM D,L-homocysteine. 5 In conclusion, an acute infusion of homocysteine altered acetylcholine endothelium-induced vasodilatation, whereas the adenosine vasodilatator effect was insensitive to the deleterious action ofhomocysteine in vitro.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 16/07/20 alle ore 05:59:50