[Lysophosphatidic acid activates L-arginine/nitric oxide pathway of platelets in rats].
Beijing Da Xue Xue Bao Yi Xue Ban
; 37(6): 603-7, 2005 Dec 18.
Article
en Zh
| MEDLINE
| ID: mdl-16378111
OBJECTIVE: To investigate the mechanism of platelet function caused by Lysophosphatidic acid (LPA), by observing the change of the L-arginine/nitric oxide synthase/nitric oxide (L-Arg/NOS/NO) pathway of platelet in rats. METHODS: LPA (10(-6), 10(-5) and 5x10(-5) mol/L) was administrated in rats and incubated for 30 and 60 minutes. The nitrite production was measured by Greiss assay; NOS activities and L-arginine transportation were detected by isotope tracer method and intracellular [Ca(2+)]i changes by fluorescent probe. RESULTS: LPA increased NO release by 35% and 56%, after incubating for 30 and 60 minutes, respectively. LPA (10(-6), 10(-5)aand 5x10(-5) mol/L) enhanced the NO productions of platelets in a concentration-dependent manner (P<0.01). EC(50) was 17.8 micromol/L, and 95% CI was 13.3-24.2 micromol/L, involved in the physiological concentration of LPA in plasma (P<0.01). Simultaneously, different doses of LPA increased NOS activities and L-arginine uptake in a dose-dependent manner (P<0.01). In this study, LPA (50 micromol/L) increased the intracellular free calcium ion concentration ([Ca(2+)]i, P<0.01), after incubating for 30 and 60 minutes. Pre-treated with NOS inhibitor-L-NAME for 20 minutes, LPA obviously enhanced the effects by 20% and 32% respectively (P<0.01). On the contrary, pre-treated with L-arginine (200 micromol/L) for the same times obviously reduced the effects by 14% and 18% respectively (P<0.01). CONCLUSION: LPA increased NO release by enhancing L-arginine uptake and NOS activities, up-regulating L-arginine/NOS/NO pathway in platelets of rats.
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Colección:
01-internacional
Base de datos:
MEDLINE
Asunto principal:
Arginina
/
Plaquetas
/
Lisofosfolípidos
/
Óxido Nítrico
Límite:
Animals
Idioma:
Zh
Revista:
Beijing Da Xue Xue Bao Yi Xue Ban
Asunto de la revista:
MEDICINA
Año:
2005
Tipo del documento:
Article
País de afiliación:
China
Pais de publicación:
China