Abstract
Lepidium sativum is widely used in folk medicine for treatment of hyperactive airways disorders, such as asthma, bronchitis and cough. The crude extract of Lepidium sativum (Ls.Cr) inhibited carbachol (CCh, 1 mu M-) and K+ (80 mM-) induced contractions in a pattern similar to that of dicyclomine. Ls.Cr at 0.03 mg/mL produced a rightward parallel shift of CCh curves, followed by nonparallel shift at higher concentration (0.1 mg/mL), suppressing maximum response, similar to that caused by dicyclomine. Pretreatment of tissues with Ls.Cr (0.1-0.3 mg/mL) shifted Ca++ concentration-response curves (CRCs) to right, as produced by verapamil. Ls.Cr at low concentrations (0.03-0.1 mg/mL) caused leftward shift of isoprenaline-induced inhibitory CRCs, like that caused by rolipram, a phosphodiesterase (PDE) inhibitor. These results indicate that bronchodilatory effect of Lepidium sativum is mediated through a combination of anticholinergic, Ca++ antagonist and PDE inhibitory pathways, which provides sound mechanistic background for its medicinal use in the overactive airways disorders.