Vasorelaxant properties of Vernonia amygdalina ethanol extract and its possible mechanism.

Context: Vernonia amygdalina Del. (VA) (Asteraceae) is commonly used to treat hypertension in Malaysia.

Objective: This study investigates the vasorelaxant mechanism of VA ethanol extract (VAE) and analyzes its tri-step FTIR spectroscopy fingerprint.

Materials And Methods: Dried VA leaves were extracted with ethanol through maceration and concentrated using rotary evaporator before freeze-dried. The vasorelaxant activity and the underlying mechanisms of VAE using the cumulative concentration (0.01-2.55 mg/mL at 20-min intervals) were evaluated on aortic rings isolated from Sprague Dawley rats in the presence of antagonists.

Results: The tri-step FTIR spectroscopy showed that VAE contains alkaloids, flavonoids, and saponins. VAE caused the relaxation of pre-contracted aortic rings in the presence and absence of endothelium with EC of 0.057 ± 0.006 and 0.430 ± 0.196 mg/mL, respectively. In the presence of Nω-nitro-l-arginine methyl ester (EC 0.971 ± 0.459 mg/mL), methylene blue (EC 1.203 ± 0.426 mg/mL), indomethacin (EC 2.128 ± 1.218 mg/mL), atropine (EC 0.470 ± 0.325 mg/mL), and propranolol (EC 0.314 ± 0.032 mg/mL), relaxation stimulated by VAE was significantly reduced. VAE acted on potassium channels, with its vasorelaxation effects significantly reduced by tetraethylammonium, 4-aminopyridine, barium chloride, and glibenclamide (EC 0.548 ± 0.184, 0.158 ± 0.012, 0.847 ± 0.342, and 0.304 ± 0.075 mg/mL, respectively). VAE was also found to be active in reducing Ca released from the sarcoplasmic reticulum and blocking calcium channels.

Conclusions: The vasorelaxation effect of VAE involves upregulation of NO/cGMP and PGI signalling pathways, and modulation of calcium/potassium channels, and muscarinic and β-adrenergic receptor levels.