veratrine and peoniflorin

In this study, we attempted to identify the interactions and mechanisms between veratrine and paeoniflorin on isolated mouse vas deferens. Paeoniflorin had no effect on isolated mouse vas deferens. Veratrine (1 x 10(-5) approximately 1 x 10(-3) g/ml) could directly induce contraction of isolated rat and mouse vas deferens. The concentration induced by veratrine (1 x 10(-5) g/ml) was completely inhibited by Ca2+-free solution and verapamil (1 x 10(-5) M), in both the epididymal and the prostatic portions of isolated mouse vas deferens. Naloxone (1 x 10(-5) M) did not alter the contraction induced by veratrine (1 x 10(-5) g/ml) in either the epididymal or the prostatic portions of isolated mouse vas deferens. Paeoniflorin (4.8 x 10(-5) g/ml) inhibited the contraction induced by veratrine (1 x 10(-5) g/ml) in both the epididymal and the prostatic portions of isolated mouse vas deferens. Paeoniflorin (4.8 x 10(-5) g/ml) potentiated norepinephrine (1 x 10(-5) M)-induced phasic contraction in the epididymal portion, but decreased contractions in the prostatic portion. Paeoniflorin (4.8 x 10(-5) g/ml) increased KCI (56 mM)-induced phasic contraction in the epididymal portion, but decreased the tonic contraction in either the epididymal or the prostatic portion. Veratrine (1 x 10(-5) g/ml)-induced contractions could be decreased by pretreatment with ryanodine (1 x 10(-5) M) in both the epididymal and the prostatic portions. Pretreatment with the combination of paeoniflorin (4.8 x 10(-5) g/ml) and ryanodine (1 x 10(-5) M) did not potentiate the inhibition of paeoniflorin in the veratrine-induced contraction in both the epididymal and the prostatic portions of isolated mouse vas deferens.

Topics: Animals; Anti-Inflammatory Agents, Non-Steroidal; Benzoates; Bridged-Ring Compounds; Calcium Channel Blockers; Dose-Response Relationship, Drug; Drug Interactions; Glucosides; Male; Mice; Mice, Inbred ICR; Monoterpenes; Muscle Contraction; Norepinephrine; Phytotherapy; Plant Extracts; Ryanodine; Time Factors; Vas Deferens; Veratrine; Veratrum

The interactions and mechanisms between veratrine and paeoniflorin on the isolated rat aorta were studied. Veratrine (1x10(-6) to 1x10(-4) g/ml) could induce contraction on the isolated rat aorta in a concentration-related manner. Paeoniflorin had no effect on the isolated rat aorta. Pretreatment with prazosin (1x10(-6) M) and nifedipine (1x10(-6) M) but not yohimbine (1x10(-5) M) could decrease the tension of contraction induced by veratrine (1x10(-4) g/ml). Sodium nitroprusside (1x10(-4) M) could inhibit the contraction induced by veratrine (1x10(-4) g/ml) with or without endothelium, whereas methylene blue (5x10(-5) M) could increase the contraction induced by veratrine (1x10(-4) g/ml). Treatment with veratrine (1x10(-4) g/ml) could decrease the tension of contraction induced by norepinephrine (1x10(-6) M) or phenylephrine (1x10(-4) M). The inhibition of veratrine on norepinephrine-induced contraction was potentiated by L-arginine (1x10(-4) M) and reversed by L-NAME (1x10(-5) M). Paeoniflorin (1x10(-4) M) could decrease the tension of contraction induced by veratrine (1x10(-4) g/ml) and methylene blue (5x10(-5) M). The inhibition of paeoniflorin on veratrine was more potent on rat isolated aorta with endothelium than without endothelium. Ryanodine (1x10(-5) M) and Ca2+ -free medium could inhibit methylene blue-induced contraction. From the above results, the relaxation of veratrine on the norepinephrine-induced contraction might be related to the increase of NO and cGMP. The contraction of veratrine on the isolated rat aorta was via the increase of intracellular calcium which was inhibited by paeoniflorin.

Topics: Animals; Anti-Inflammatory Agents, Non-Steroidal; Aorta, Thoracic; Benzoates; Bridged-Ring Compounds; Calcium; Drug Interactions; Endothelium; Glucosides; In Vitro Techniques; Male; Monoterpenes; Norepinephrine; Rats; Rats, Sprague-Dawley; Time Factors; Vasoconstrictor Agents; Veratrine

In this study, we attempted to identify the interactions and mechanisms between veratrine and paeoniflorin on isolated rat atria. Paeoniflorin alone showed no effect on the rat atria. Veratrine increased the atrial contraction and induced arrhythmia at 1 x 10(-5) g/ml. Veratrine could directly induce contraction and elicit tetanic contraction at 1 x 10(-4) g/ml in the left atria with or without electric stimulation. Paeoniflorin (4.8 x 10(-6) to 4.8 x 10(-3) g/ml), verapamil (2.2 x 10(-6) g/ml), tetrodotoxin (TTX) (3.2 x 10(-8) g/ml) and quinidine (7.5 x 10(-6) g/ml) inhibited the increase of contraction and delayed the onset of contraction induced by veratrine (1 x 10(-5) g/ml). The inhibitory effect of paeoniflorin combined with verapamil on the contraction induced by veratrine was more potent than that of paeoniflorin or verapamil alone. However, the inhibitory effect of paeoniflorin was not potentiated by TTX or quinidine. From the above results, the contraction evoked by veratrine in the rat atria may be concluded to be caused by the stimulation of Na(+)- and Ca(2+)-ion channels. The inhibition of paeoniflorin on the contraction induced by veratrine may primarily be related to the blockade of Ca2+ channels.

Topics: Animals; Arrhythmias, Cardiac; Benzoates; Bridged-Ring Compounds; Calcium Channels; Glucosides; Heart Atria; Herb-Drug Interactions; In Vitro Techniques; Male; Monoterpenes; Myocardial Contraction; Phytotherapy; Plant Extracts; Plants, Medicinal; Rats; Rats, Wistar; Sodium Channels; Time Factors; Veratrine