ArticleAmerican journal of physiology. Heart and circulatory physiology2008
Tricyclic antidepressant amitriptyline alters sarcoplasmic reticulum calcium handling in ventricular myocytes.
Article in American journal of physiology. Heart and circulatory physiology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 28 citations in OpenAlex.
- Impact of mental disorders on the risk of heart failure among Korean patients with diabetes: a cohort study.Cardiovascular diabetology · 2023Article
- Nebivolol suppresses cardiac ryanodine receptor-mediated spontaneous Ca2+ release and catecholaminergic polymorphic ventricular tachycardia.The Biochemical journal · 2016Article
- R-CEPIA1er as a new tool to directly measure sarcoplasmic reticulum [Ca] in ventricular myocytes.American journal of physiology. Heart and circulatory physiology · 2016Article
- Approaching ryanodine receptor therapeutics from the calcin angle.The Journal of general physiology · 2016Article
- Drug elucidation: invertebrate genetics sheds new light on the molecular targets of CNS drugs.Frontiers in pharmacology · 2014Review
- Potential role of cardiac calsequestrin in the lethal arrhythmic effects of cocaine.Drug and alcohol dependence · 2013Article
- Calsequestrin 2 and arrhythmias.American journal of physiology. Heart and circulatory physiology · 2012Review
- Single ryanodine receptor channel basis of caffeine's action on Ca2+ sparks.Biophysical journal · 2011Article
- Early and prolonged ECG alterations resembling a myocardial injury after severe amitriptyline poisoning.HSR proceedings in intensive care & cardiovascular anesthesia · 2010Article
- Trifluoperazine: a rynodine receptor agonist.Pflugers Archiv : European journal of physiology · 2009Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Tricyclic antidepressants such as amitriptyline (AMT) have been reported to have adverse side effects on cardiac performance. AMT effects on Ca handling in ventricular myocytes, however, are not well understood. Therefore, we investigated AMT action on sarcoplasmic reticulum (SR) Ca release in ventricular myocytes, ryanodine receptor (RyR) activity, and Ca uptake by SR microsomes. In permeabilized myocytes, AMT transiently increased free luminal Ca concentration ([Ca]) followed by marked depletion. AMT (10 microM) caused a rapid and a transient increase of Ca spark frequency, followed by a significant suppression of spark activity. The latter was associated with a decrease of Ca spark amplitude and SR Ca load to 87 and 60%, respectively. AMT (10 microM) completely abolished propagation of spontaneous Ca waves. Higher concentrations of AMT (0.1-1 mM) evoked SR Ca release reminiscent of the effect of caffeine (20 mM) and caused almost complete depletion of SR Ca content. Studies on single calsequestrin-free RyR channels revealed that AMT increased the mean open time and open probability (Po) in a dose-dependent fashion (dissociation constant = 4.2 microM). High concentrations of AMT (> 25 microM) evoked frequent long openings with Po reaching very high levels (> 0.70). In studies with cardiac SR microsomes, AMT slowed the rate of ATP-dependent Ca uptake. We conclude that AMT affects SR Ca handling in ventricular myocytes by multiple mechanisms, including direct stimulation of RyRs and inhibition of SR Ca uptake. These effects could contribute to AMT cardiotoxicity.
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