Vasorelaxant effects of Brillantaisia nitens Lindau (Acanthaceae) extracts on isolated rat vascular smooth muscle

Brillantaisia nitens Lindau (Acanthaceae) is traditionally used in Cameroon for the treatment of many diseases including cardiovascular disorders. We have studied its vasorelaxant effects in rat vascular smooth muscle. In this study, aqueous, methylene chloride, methanol, and methylene chloride/methanol leaves extracts of Brillantaisia nitens were tested for their relaxing ability in vitro. Strips of rat aorta, with or without intact endothelium, were mounted in tissue baths, contracted with KCl (60 mM) or norepinephrine (10−4 M), and then exposed to the plant extracts. These extracts exhibited concentration-dependent vasorelaxations of norepinephrine-induced contractions of intact aortic strips. The EC50 were 0.42 ± 0.01 mg/ml (aqueous extract), 0.63 ± 0.02 mg/ml (methylene chloride extract), 0.73 ± 0.02 mg/ml (methanol extract) and 0.36 ± 0.02 mg/ml (methylene chloride/methanol extract). The methylene chloride/methanol (CH2Cl2/CH3OH) extract was the most potent relaxing extract. It caused a concentration-dependent and endothelium-independent relaxation of the rat aortic strips contracted by KCl or norepinephrine. On the NE-induced contraction, its maximal relaxant activity (109%) due to the dose of 1.5 mg/ml, was not significantly modified by the pretreatment of aortic strips with indomethacin (89%, P > 0.05) or with l-NAME (103%, P > 0.05). This suggests that the vasorelaxation elicited by CH2Cl2/CH3OH extract was not mediated via endothelium-derived prostacyclin or nitric oxide. In contrast, this relaxation was markedly reduced by tetraethylammonium, a blocker of non-selective K+ channels and glibenclamide, a blocker of ATP-sensitive K+ channels. The CH2Cl2/CH3OH extract significantly inhibited Ca2+-induced concentration-contraction and the Ca2+ influx in aortic strips incubated with 60 mM KCl. These results indicate that the vasorelaxant effect of the CH2Cl2/CH3OH extract of Brillantaisia nitens is due to an inhibition of Ca2+ influx, possibly via the activation of ATP-sensitive K+ channels.