Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0231530 (twitching)
 2,043 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

1. The present study compares the effects of verapamil and Bay K 8644 on twitches of the mouse vas deferens induced by field stimulation at 0.1 Hz. The influence of interactions between these drugs and nifedipine on neurotransmission was also investigated. 2. Bay K 8644 (0.1 nM-3 microM) and verapamil (1-100 microM) potentiated twitches maximally by about 1000% (EC50 17.3 nM) and 300% (EC50 17.5 microM), respectively. Nifedipine (0.1 nM-1 microM) only reduced twitch magnitude (IC50 7.7 nM). All effects were reversed following washout. 3. Yohimbine (1-100 microM) reversed twitch potentiation caused by verapamil but not by Bay K 8644. Prazosin (1 microM) did not reduce basal twitch tension nor antagonize twitch potentiation by verapamil. 4. Twitch inhibition by nifedipine was unaltered by previous incubation with verapamil (30 microM), but Bay K 8644 (1 microM) shifted the curve to nifedipine 120 fold to the right. Previous incubation with nifedipine (1 microM) blocked potentiation induced by verapamil but did not modify responsiveness to Bay K 8644. 5. Previous addition of verapamil (30 microM) markedly enhanced twitch potentiation caused by Bay K 8644 in a supra-additive fashion. In experiments conducted in the reversed condition, Bay K 8644 (1 nM but not 10 nM) potentiated the effect of verapamil in a similar manner but to a lesser extent. 6. It is concluded that verapamil, in contrast to nifedipine, markedly enhances neurally-evoked twitches of the mouse vas deferens. Bay K 8644 produces essentially the same effect as verapamil, but its potency is 1000 fold and its maximal effect about 3 fold greater than that observed for verapamil. It is suggested that the mechanism of twitch potentiation by verapamil is different from that of Bay K 8644 and may involve an increased release of non-adrenergic co-transmitter(s).
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PMID:Interactions of calcium antagonists and the calcium channel agonist Bay K 8644 on neurotransmission of the mouse isolated vas deferens. 246 18

Effects of agents with selectivity for the alpha1- or alpha2-adrenoceptor have been investigated on the head twitches induced by 5-HT injected into the cerebral ventricles in the mouse. Alpha-adrenoceptor agonists inhibited head-twitching with a rank order of potency: guanabenz, clonidine, phenylephrine, methoxamine. The antagonists yohimbine and piperoxane, potentiated the head-twitch frequency. These results suggest that there may be an involvement of an alpha2-adrenoceptor. Small doses of phenylephrine (s.c.) potentiated the head-twitch. Methoxamine, injected intracerebroventricularly potentiated the head-twitch only when alpha2-adrenoceptors were blocked by a small dose of yohimbine. Prazosin and thymoxamine inhibited the head-twitch, suggesting that alpha1-adrenoceptors also modulate this phenomenon. Yohimbine and phenylephrine increased the incidence of spontaneous head-twitches. A tonic noradrenergic input may be necessary for the occurrence of the head-twitch induced by 5-HT.
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PMID:Effects on the 5-hydroxytryptamine-induced head-twitch of drugs with selective actions on alpha1 and alpha2-adrenoceptors. 612 9

The effects of the dopamine antagonists haloperidol and sultopride were investigated on the twitch response, evoked by 0.1 Hz stimulation of guinea-pig isolated ileal longitudinal muscle, and on the inhibition of the twitch response induced by 10 Hz stimulation (post-tetanic twitch inhibition) and by application of opioids. Both haloperidol and sultopride concentration-dependently inhibited the twitch response, with threshold concentrations of 2 and 50 microM, respectively, and could also shift the concentration-response curve for ACh-contraction to the right in a non-competitive manner. Haloperidol (1 microM) and sultopride (20 microM) increased post-tetanic twitch inhibition and this could be prevented by naloxone (100 nM). Twitch inhibition induced by morphine and dynorphin 1-13 was not affected by haloperidol (1 microM) or sultopride (20 microM). Prazosin (1 microM) and yohimbine (2 microM) did not affect either the twitch response or the post-tetanic twitch inhibition. These results suggest that dopamine receptors are involved in the modulation of the ileal opioid system, in such a manner as to diminish the release of endogenous opioids by tetanic stimulation.
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PMID:The dopaminergic system modulates the endogenous opioid system in guinea-pig isolated ileal longitudinal muscle. 756 80