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Possible mechanisms involved in the effect of the subchronic administration of rosuvastatin on endothelial function in rats with metabolic syndrome.
Lozano-Cuenca, J; Valencia-Hernández, I; López-Canales, O A; Flores-Herrera, H; López-Mayorga, R M; Castillo-Henkel, E F; López-Canales, J S.
Afiliación
  • Lozano-Cuenca J; Department of Physiology and Cell Development, National Institute of Perinatology, Mexico City, Mexico.
  • Valencia-Hernández I; Section of Postgraduate Studies and Investigation, Higher School of Medicine, National Polytechnic Institute, Mexico City, Mexico.
  • López-Canales OA; Section of Postgraduate Studies and Investigation, Higher School of Medicine, National Polytechnic Institute, Mexico City, Mexico.
  • Flores-Herrera H; Department of Immuno-Biochemistry, National Institute of Perinatology, Mexico City, Mexico.
  • López-Mayorga RM; Section of Postgraduate Studies and Investigation, Higher School of Medicine, National Polytechnic Institute, Mexico City, Mexico.
  • Castillo-Henkel EF; Section of Postgraduate Studies and Investigation, Higher School of Medicine, National Polytechnic Institute, Mexico City, Mexico.
  • López-Canales JS; Department of Physiology and Cell Development, National Institute of Perinatology, Mexico City, Mexico.
Braz J Med Biol Res ; 53(2): e9304, 2020.
Article en En | MEDLINE | ID: mdl-32049102
Metabolic syndrome is a multifaceted condition associated with a greater risk of various disorders (e.g., diabetes and heart disease). In a rat model of metabolic syndrome, an acute in vitro application of rosuvastatin causes relaxation of aortic rings. Since the outcome of a subchronic rosuvastatin treatment is unknown, the present study explored its effect on acetylcholine-induced vasorelaxation of aortic rings from rats with metabolic syndrome. Animals were submitted to a 16-week treatment, including a standard diet, a cafeteria-style diet (CAF-diet), or a CAF-diet with daily rosuvastatin treatment (10 mg/kg). After confirming the development of metabolic syndrome in rats, aortic segments were extracted from these animals (those treated with rosuvastatin and untreated) and the acetylcholine-induced relaxant effect on the corresponding rings was evaluated. Concentration-response curves were constructed for this effect in the presence/absence of L-NAME, ODQ, KT 5823, 4-aminopyridine (4-AP), tetraethylammonium (TEA), apamin plus charybdotoxin, glibenclamide, indomethacin, clotrimazole, and cycloheximide pretreatment. Compared to rings from control rats, acetylcholine-induced vasorelaxation decreased in rings from animals with metabolic syndrome, and was maintained at a normal level in animals with metabolic syndrome plus rosuvastatin treatment. The effect of rosuvastatin was inhibited by L-NAME, ODQ, KT 5823, TEA, apamin plus charybdotoxin, but unaffected by 4-AP, glibenclamide, indomethacin, clotrimazole, or cycloheximide. In conclusion, the subchronic administration of rosuvastatin to rats with metabolic syndrome improved the acetylcholine-induced relaxant response, involving stimulation of the NO/cGMP/PKG/Ca2+-activated K+ channel pathway.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Aorta / Vasodilatación / Endotelio Vascular / Acetilcolina / Síndrome Metabólico / Rosuvastatina Cálcica Límite: Animals Idioma: En Revista: Braz J Med Biol Res Año: 2020 Tipo del documento: Article País de afiliación: México Pais de publicación: Brasil
Texto completo
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Aorta / Vasodilatación / Endotelio Vascular / Acetilcolina / Síndrome Metabólico / Rosuvastatina Cálcica Límite: Animals Idioma: En Revista: Braz J Med Biol Res Año: 2020 Tipo del documento: Article País de afiliación: México Pais de publicación: Brasil