Anemoside A3-induced Relaxation in Rat Renal Arteries: Role of Endothelium and Ca2+ Channel Inhibition

Anemoside A 3 , a lupane-type triterpenoid saponin, exists in the roots of PULSATILLA CHINENSIS, but its pharmacological properties are largely unknown. The present study aimed to investigate the mechanisms underlying anemoside A 3 -induced relaxation in rat renal arteries. Changes of isometric force were determined on arteries with a myograph. Anemoside A 3 caused concentration-dependent relaxation in precontracted aortas, mesenteric, left coronary, and renal arteries. Removal of endothelium or treatment with charybdotoxin plus apamin slightly but significantly attenuated the relaxation in renal arteries. TEA + inhibited the relaxation caused by anemoside A 3 in renal arteries with and without endothelium while glibenclamide, BaCl 2 , or capsaicin had no effect on it. Anemoside A 3 produced less relaxation in rings contracted by 60 mM KCl compared with rings contracted by receptor-dependent constrictors. It further inhibited contractions induced by Ca 2+ influx through nifedipine-sensitive voltage-gated Ca 2+ channels, nifedipine-insensitive receptor-operated Ca 2+ channels, and by intracellular Ca 2+ release. Pretreatment with nifedipine attenuated anemoside A 3 -induced relaxation. Taken together, the present results indicate that anemoside A 3 produces relaxation in rat renal arteries through multiple mechanisms. The release of CTX/apamin-sensitive endothelium-derived hyperpolarizing factor, stimulation of TEA + -sensitive K + channel, and inhibition of Ca 2+ influx jointly contribute to the relaxation.