<i>Terminalia glaucescens</i> ethanol stem extract induces vasorelaxation via nitric oxide/guanylyl cyclase/cyclic guanosine monophosphate pathway in the aortic smooth muscle of male Wistar rats

Blood vessels contain vascular smooth muscle that responds to various agonists and endothelial cells essential for maintaining vascular homeostasis. Studies have explored the vasorelaxant effects of Terminalia species but not Terminalia glaucescens. This study investigates the endothelium-dependent activities of ethanol stem extract of Terminalia glaucescens (ESET) on the aortic smooth muscle (ASM) of male Wistar rats. Aortic smooth muscle from male Wistar rats weighing 150-200 g was removed and mounted in 50-mL jacketed tissue baths containing physiological salt solution connected to a force transducer to measure the isometric contraction. The relaxation activity of ESET after precontraction of the ASM by phenylephrine (PHE) and potassium chloride (KCl) was investigated. ASM was preincubated with ESET, and contractile response to PHE, KCl, acetylcholine and sodium nitroprusside (SNP) was observed. Furthermore, the vasorelaxant activities of ESET after mechanical removal of the endothelium, pre-incubation with L-NG-Nitro arginine methyl ester (L-NAME), methylene blue (MB), and indomethacin were determined. ESET significantly reduces (p<0.05) ASM contraction response to PHE and relaxed ASM precontracted with PHE and KCl. ESET improved relaxation (%) response to acetylcholine and SNP. The endothelium removal significantly reduced the ASM relaxation response to SNP in the presence of ESET. The vasorelaxant effect caused by the extract was significantly (p<0.05) reduced with pre-incubation of the ASM with MB, enhanced by indomethacin and not affected by L-NAME. The action of ethanol stem extract of Terminalia glaucescens is endothelium-dependent and involves the NO/guanylyl cyclase/cyclic guanosine monophosphate pathway