ArticleBritish journal of pharmacology1993
Blockade by calmodulin inhibitors of Ca2+ channels in smooth muscle from rat vas deferens.
Article in British journal of pharmacology, 1993. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 41 citations in OpenAlex.
- Sigma-1 Receptor Ligands Chlorpromazine and Trifluoperazine Attenuate CaCell and tissue biology · 2022Article
- Bilobal architecture is a requirement for calmodulin signaling to CaProceedings of the National Academy of Sciences of the United States of America · 2018Article
- Trifluoperazine Attenuates Store-Dependent CaDoklady. Biochemistry and biophysics · 2018Article
- Cardiac contractile dysfunction during acute hyperglycemia due to impairment of SERCA by polyol pathway-mediated oxidative stress.American journal of physiology. Cell physiology · 2010Article
- Polyol pathway impairs the function of SERCA and RyR in ischemic-reperfused rat hearts by increasing oxidative modifications of these proteins.Journal of molecular and cellular cardiology · 2010Article
- Short-term synaptic depression and recovery at the mature mammalian endbulb of Held synapse in mice.Journal of neurophysiology · 2008Article
- Modulation of a voltage-gated calcium channel linked to activation of glutamate receptors and calcium-induced calcium release in the catfish retina.The Journal of physiology · 2001Article
- Inhibition of a mammalian large conductance, calcium-sensitive K+ channel by calmodulin-binding peptides.The Journal of physiology · 2000Article
- Role of calmodulin in the activation of carbachol-activated cationic current in guinea-pig gastric antral myocytes.Pflugers Archiv : European journal of physiology · 1995Article
- Inhibition of olfactory cyclic nucleotide-activated current by calmodulin antagonists.British journal of pharmacology · 1994Article
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
1. Effects of three compounds which are used as calmodulin inhibitors (trifluoperazine, W-7 and calmidazolium) on Ca2+ channels were investigated in smooth muscle from rat vas deferens. 2. All three calmodulin inhibitors relaxed the smooth muscle precontracted by a high concentration of KCl (63.7 mM). The order of potency for the relaxation was trifluoperazine > W-7 > calmidazolium. 3. In binding studies using a microsomal fraction of vas deferens, all these calmodulin inhibitors displaced specific [3H]-nimodipine binding. Trifluoperazine and W-7 inhibited the binding at concentrations that relaxed the smooth muscle whereas calmidazolium inhibited at concentrations much lower than those necessary for muscle relaxation. 4. Ba2+ current flowing through voltage-gated Ca2+ channels was measured under whole-cell voltage-clamp conditions in isolated smooth muscle cells. The Ba2+ current was suppressed by the three calmodulin inhibitors in the concentration-range where inhibition of [3H]-nimodipine binding was observed. Neither voltage-dependence nor the inactivation time course of Ba2+ current were affected by these compounds. 5. The results suggest that the calmodulin inhibitors directly block Ca2+ channels in the smooth muscle cells. The channel inhibition by trifluoperazine and W-7, but perhaps not that by calmidazolium, may be responsible for the muscle relaxation observed with these compounds.
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