Uterine muscle contraction is dependent on external Ca2+ and Ca2+ release from cytoplasmic storage sites. In this study, the mechanism of Ca2+ mobilization in uterine muscle cells by glycoside, dalsaxini, isolated from the root of D. Saxatilis was investigated in the rat. Uterine muscle contractility stimulated by dalsaxin was concentration dependent (ED50 0.13 mg/ml) and was significantly attenuated (85%; P < 0.01) in Ca(2+)-free physiological solution and in solutions containing verapamil (0.06-0.48 mumol). The small transient contraction observed in Ca(2+)-free medium was further suppressed by caffeine (2 mmol) and completely abolished in solutions containing Lanthanum chloride [(La3+), 2 mmol]. Contractions stimulated by the glycoside were unaffected by amiloride (50-83 mumol) in Ca(2+)-free and Ca(2+)-containing media. Dalsaxin also altered the pattern of uterine contraction stimulated by high potassium depolarization from fast-phasic to a sustained but transient plateau. It is concluded that dalsaxin causes uterine muscle contraction by mobilizing external Ca2+ through predominantly a voltage-dependent Ca2+ channel.
Indian journal of physiology and pharmacology 04/1999; 43(2):171-8.