Skeletal muscle relaxant properties of the aqueous extract of Portulaca oleracea.

The skeletal muscle relaxant properties of an aqueous extract of Portulaca oleracea were examined on the twitch and tetanus tension evoked by electrical stimulation using the rat phrenic nerve-hemidiaphragm and frog sciatic nerve-sartorius muscle preparations and on contractures induced by nicotinic agonists using the rat rectus abdominis muscle preparation. The extract (5-50 X 10(-4) g/ml) produced a dose-dependent initial enhancement, followed by a longer lasting depression of twitch tension as induced by indirect electrical stimulation (NS) as well as direct stimulation (MS) of the diaphragm and sartorius muscle preparations. The augmentation of twitch amplitude (MS) produced by the extract was not significantly antagonised or potentiated by d-tubocurarine (5-50 X 10(-8) M) or physostigmine (5-50 X 10(-8) M) at concentrations which blocked or potentiated NS-induced twitch contractions. Furthermore, tetrodotoxin (5 X 10(-7) g/ml) alone or in combination with d-tubocurarine did not significantly attenuate extract-induced augmentation of twitch contractions to MS. In addition, the depression of twitch tension due to NS was not antagonised by physostigmine but was reversed and/or abolished by Ca2+ (2-5 X 10(-3) M) or potassium thiocyanate (1 X 10(-3) M). Contractures induced by K+ (80 mM) or by tetanic stimulation (20-60 Hz) were significantly reduced by the extract whereas, contracture induced by caffeine (2.5-6.0 mM) was not affected. Ca2+-free Tyrode's solution and EDTA (1.25 X 10(-3) g/ml) potentiated extract-induced depression of twitch tension to MS. On the rectus abdominis, contractures induced by nicotinic agonists (acetylcholine, 3-500 X 10(-7) M; carbachol, 5-500 X 10(-7) M and nicotine, 5-500 X 10(-8) M) were significantly attenuated and/or abolished by the extract (5-10 X 10(-3) g/ml). These observations indicate that the aqueous extract possesses unique skeletal muscle relaxant properties which do not appear to involve interference with cholinoceptor mechanism(s). It appears that the mechanism of action of the extract may involve interference with Ca2+ mobilization in skeletal muscle.