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The aim of this study was to investigate the vasorelaxant effect of hydro-ethanol bark extract of Adansonia digitata (ADE) in porcine coronary arteries and to revealed mechanism of this effect. ADE has produced 100 % relaxation at 100 µg/ml dose in endothelium intact arteries pre-contracted by U46619. This effect was abolished by mechanical removal of endothelium. Different inhibitors were used to investigate the mechanism of vasorelaxation. L-nitro-arginin (L-NA) an inhibitor of endothelial NO synthase; MnTMPyP, an inhibitor of intracellular production reactive oxygen species and Wortmannin, an inhibitor of redox-sensitive pathway PI3 kinase/Akt Src has significantly reduced vasorelaxant effect of ADE whereas indomethacin (INDO), cyclooxygenase inhibitor; the apamin (APA) an inhibitor of small conductance potassium channels calcium-dependent (SKCa) and TRAM an inhibitor of intermediary conductance potassium channels calcium-dependent (IKCa) have no effect on vasorelaxation produced by ADE. Bradykinin was used to verify the presence of a functional endothelium. The results have shown that the ADE induces a redox-sensitive endothelium-dependent relaxation mediated by NO whereas prostacyclins and endothelium-derived hyperpolarizing factors (EDHF) have not appeared to play a role in the vascular effects. Hence, Adansonia digitata induces vasodilation which explain its antihypertensive effect and its use in traditional African medicine.
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