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Withania somnifera ameliorates lead-induced augmentation of adrenergic response in rat portal vein

OBJECTIVES: Present study was undertaken to elucidate the ameliorating potential of Withania somnifera root extract (WRE) against lead-induced augmentation of adrenergic response in rat portal vein. MATERIALS AND METHODS: In-vitro studies were conducted on effect of lead alone and lead+WRE on rat-is...

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Detalles Bibliográficos
Autores principales: Hore, Subrata Kumar, Choudhury, Soumen, Ahmad, Abul Hasan, Garg, Satish Kumar
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Medknow Publications & Media Pvt Ltd 2013
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3847244/
https://www.ncbi.nlm.nih.gov/pubmed/24347762
http://dx.doi.org/10.4103/0253-7613.121365
Descripción
Sumario:OBJECTIVES: Present study was undertaken to elucidate the ameliorating potential of Withania somnifera root extract (WRE) against lead-induced augmentation of adrenergic response in rat portal vein. MATERIALS AND METHODS: In-vitro studies were conducted on effect of lead alone and lead+WRE on rat-isolated portal vein while in-vivo studies were done in three groups of 12 rats each; Group-II and III received 0.5% lead acetate and 1.0% WRE + 0.5% lead acetate, respectively, in drinking water for 12 weeks whereas group-I served as control. Adrenaline and noradrenaline levels in brain and blood were determined by HPLC assay while vascular reactivity of portal vein to lead and WRE was determined by measuring the isometric tension. RESULTS: Following in-vitro exposure, lead did not alter the contractile effect of phenylephrine. In-vivo studies revealed that contractile effect of lead on portal vein was significantly potentiated and it was antagonized by prazosin (10(-7) M) and WRE (1%). WRE treatment significantly reduced elevated blood noradrenaline (37.80%) and restored noradrenaline level in brain (39.39%) in lead-exposed animals. These values were almost comparable to the control group. But it failed to significantly affect the blood and brain adrenaline levels. CONCLUSIONS: Results suggest that following pre-exposure of rats to WRE, lead-induced augmentation of alpha(1)-adrenoceptors mediated response was reversed possibly by regulating catecholamine release from nerve endings. Thus, WRE may be useful in therapeutic management of lead-induced hypertension.