Mechanisms of Kaempferia parviflora extract (KPE)- induced vasorelaxation in the rat aorta

AbstractBackground: The rhizomes of Kaempferia parviflora (KP) have been widely used in Thai traditional medicine to treat several diseases such as hypertension. Recent studies have shown that the ethanolic extract of KP (KPE) exerts vasorelaxant effects in the rat aorta. However, the underlying mechanisms of these vascular responses remain unclear. Objectives: Investigate the mechanisms of KPE-induced vasorelaxation in the rat aorta. Methods: Aortic rings from male Wistar rats were precontracted with methoxamine. Changes in tension were measured using an isometric force transducer and recorded on the MacLab recording system. Vasorelaxation to KPE was examined in the presence of 10 μM indomethacin, 300 μM NG-nitro L-arginine methyl ester (L-NAME), 60 mM KCl, 5 mM tetraethylammonium chloride (TEA), 10 μM glibenclamide, 1 mM 4-aminopyridine (4-AP) or 30 μM barium chloride (BaCl2). The effects of KPE on vascular responses to carbachol, sodium nitroprusside, and CaCl2were evaluated. Results: KPE (0.1-100 μg/mL) caused vasorelaxations, which were reduced with removal of the endothelium. In addition, indomethacin, L-NAME, and indomethacin plus L-NAME reduced KPE-induced vasorelaxation. Raising the extracellular KCl concentration to 60 mM, or pre-treatment with BaCl2, TEA, or glibenclamide reduced relaxant responses to KPE. Contractions to CaCl2were inhibited after pre-incubation with KPE. Pre-treatment with KPE enhanced endothelium-dependent relaxations to carbachol, but not to sodium nitroprusside. Conclusion: KPE had a vasodilator effect in the rat isolated aortic rings. These effects involved endotheliumderived NO and prostanoids via a COX pathway. In addition, KPE-induced vasorelaxation was due to increasing K+efflux probably through KCa, KIRand KATPchannels. These provide pharmacological evidence for mechanism of KPE-induced vasorelaxation and support the traditional use of KPE as an antihypertensive agent.