ArticleThe Journal of physiology1997
Dual effects of tetracaine on spontaneous calcium release in rat ventricular myocytes.
Article in The Journal of physiology, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 77 papers.
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Who cites it
77 citing papers in PubMed, 155 citations in OpenAlex.
- The NADPH oxidase inhibitor diphenyleneiodonium suppresses CaThe Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2024Article
- Design, Synthesis, and Anticancer Evaluation of Novel Tetracaine Hydrazide-Hydrazones.ACS omega · 2023Article
- Methods to Induce Analgesia and Anesthesia in Crustaceans: A Supportive Decision Tool.Biology · 2023Review
- The use of local anaesthetics in dermatology, aesthetic medicine and plastic surgery: review of the literature.Postepy dermatologii i alergologii · 2023Review
- MATE1 Deficiency Exacerbates Dofetilide-Induced Proarrhythmia.International journal of molecular sciences · 2022Article
- Therapeutic Approaches of Ryanodine Receptor-Associated Heart Diseases.International journal of molecular sciences · 2022Review
- Article
- Increased RyR2 activity is exacerbated by calcium leak-induced mitochondrial ROS.Basic research in cardiology · 2020Article
- Targeting pathological leak of ryanodine receptors: preclinical progress and the potential impact on treatments for cardiac arrhythmias and heart failure.Expert opinion on therapeutic targets · 2020Review
- Synthesis and biological activities of local anesthetics.RSC advances · 2019Review
- Design, synthesis and biological activity evaluation of benzoate compounds as local anesthetics.RSC advances · 2019Article
- Gene Transfer of Engineered Calmodulin Alleviates Ventricular Arrhythmias in a Calsequestrin-Associated Mouse Model of Catecholaminergic Polymorphic Ventricular Tachycardia.Journal of the American Heart Association · 2018Article
- Treatment of catecholaminergic polymorphic ventricular tachycardia in mice using novel RyR2-modifying drugs.International journal of cardiology · 2017Article
- Sarcoplasmic Reticulum Structure and Functional Properties that Promote Long-Lasting Calcium Sparks.Biophysical journal · 2016Article
- Long-Lasting Sparks: Multi-Metastability and Release Competition in the Calcium Release Unit Network.PLoS computational biology · 2016Article
- Ablation of HRC alleviates cardiac arrhythmia and improves abnormal Ca handling in CASQ2 knockout mice prone to CPVT.Cardiovascular research · 2015Article
- Sensitization of cardiac Ca²⁺ release sites by protein kinase C signaling: evidence from action of murrayafoline A.Pflugers Archiv : European journal of physiology · 2015Article
- Genetic ablation of ryanodine receptor 2 phosphorylation at Ser-2808 aggravates Ca(2+)-dependent cardiomyopathy by exacerbating diastolic Ca2+ release.The Journal of physiology · 2014Article
- Calcium homeostasis in myogenic differentiation factor 1 (MyoD)-transformed, virally-transduced, skin-derived equine myotubes.PloS one · 2014Article
- Isoproterenol increases the fraction of spark-dependent RyR-mediated leak in ventricular myocytes.Biophysical journal · 2013Article
17 more citing papers are in PubMed but not listed here.
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
1. Confocal microfluorometry was used to study the effects of tetracaine on spontaneous Ca2+ release from the sarcoplasmic reticulum (SR) in isolated rat ventricular myocytes. 2. At low concentrations (0.25-1.25 mM), tetracaine caused an initial inhibition of spontaneous release events (Ca2+ sparks) and Ca2+ waves, which was followed by a gradual increase in Ca2+ release activity. The frequency and magnitude of sparks were first decreased and then increased with respect to control levels. At high concentrations (> 1.25 mM), tetracaine abolished all forms of spontaneous release. 3. Exposure of the myocytes to tetracaine resulted in a gradual increase in the SR Ca2+ load as indexed by changes in the magnitude of caffeine-induced Ca2+ transients. 4. In cardiac SR Ca(2+)-release channels incorporated into lipid bilayers, tetracaine (> 0.25 mM) induced a steady inhibition of channel activity. Addition of millimolar Ca2+ to the luminal side of the channel caused an increase in channel open probability under control conditions as well as in the presence of various concentrations of tetracaine. 5. We conclude that the primary effect of tetracaine on SR Ca(2+)-release channels is inhibition of channel activity both in vitro and in situ. The ability of tetracaine to reduce spark magnitude suggests that these events are not due to activation of single channels or non-reducible clusters of channels and, therefore, supports the multichannel origin of sparks. We propose that the paradoxical late potentiation of release by submaximal concentrations of tetracaine is caused by a gradual increase in SR Ca2+ load and subsequent activation of the Ca(2+)-release channels by Ca2+ inside the SR.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.