ArticleThe Journal of physiology1998
The effect of tetracaine on stimulated contractions, sarcoplasmic reticulum Ca2+ content and membrane current in isolated rat ventricular myocytes.
Article in The Journal of physiology, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 79 citations in OpenAlex.
- Role of ryanodine receptor cooperativity in CaThe Journal of physiology · 2024Article
- Altered calcium handling produces reentry-promoting action potential alternans in atrial fibrillation-remodeled hearts.JCI insight · 2020Article
- Exploring Impaired SERCA Pump-Caused Alternation Occurrence in Ischemia.Computational and mathematical methods in medicine · 2019Article
- Calcium and Excitation-Contraction Coupling in the Heart.Circulation research · 2017Review
- Regional acidosis locally inhibits but remotely stimulates Ca2+ waves in ventricular myocytes.Cardiovascular research · 2017Article
- Exercise training reverses myocardial dysfunction induced by CaMKIIδC overexpression by restoring Ca2+ homeostasis.Journal of applied physiology (Bethesda, Md. : 1985) · 2016Article
- Dantrolene suppresses spontaneous Ca2+ release without altering excitation-contraction coupling in cardiomyocytes of aged mice.American journal of physiology. Heart and circulatory physiology · 2014Article
- Relationship between Ca2+ sparklets and sarcoplasmic reticulum Ca2+ load and release in rat cerebral arterial smooth muscle.American journal of physiology. Heart and circulatory physiology · 2011Article
- Changes of SERCA activity have only modest effects on sarcoplasmic reticulum Ca2+ content in rat ventricular myocytes.The Journal of physiology · 2011Article
- Flecainide inhibits arrhythmogenic Ca2+ waves by open state block of ryanodine receptor Ca2+ release channels and reduction of Ca2+ spark mass.Journal of molecular and cellular cardiology · 2010Article
- Dysregulated sarcoplasmic reticulum calcium release: potential pharmacological target in cardiac disease.Pharmacology & therapeutics · 2008Review
- Removal of FKBP12.6 does not alter the conductance and activation of the cardiac ryanodine receptor or the susceptibility to stress-induced ventricular arrhythmias.The Journal of biological chemistry · 2007Article
- Origin of spontaneous rhythmicity in smooth muscle.The Journal of physiology · 2006Review
- Regulation of cardiac sarcoplasmic reticulum Ca release by luminal [Ca] and altered gating assessed with a mathematical model.Biophysical journal · 2005Article
- Calcium oscillations in interstitial cells of the rabbit urethra.The Journal of physiology · 2005Article
- A mathematical treatment of integrated Ca dynamics within the ventricular myocyte.Biophysical journal · 2004Article
- RyR2 mutations linked to ventricular tachycardia and sudden death reduce the threshold for store-overload-induced Ca2+ release (SOICR).Proceedings of the National Academy of Sciences of the United States of America · 2004Article
- The effect of acidosis on systolic Ca2+ and sarcoplasmic reticulum calcium content in isolated rat ventricular myocytes.The Journal of physiology · 2000Article
- Inhibition of Ca(2+) sparks by ruthenium red in permeabilized rat ventricular myocytes.Biophysical journal · 2000Article
- Inhibition of sarcoplasmic reticulum function by polyunsaturated fatty acids in intact, isolated myocytes from rat ventricular muscle.The Journal of physiology · 2000Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
1. The effects of tetracaine were examined on rat ventricular myocytes. In both field-stimulated and voltage-clamped cells tetracaine (100-200 microM) produced an initial decrease of contraction before a recovery towards the control level. Removal of tetracaine produced a transient overshoot of contraction to levels greater than the control. 2. The transient decrease of contraction produced by tetracaine was accompanied by a small transient increase in the integral of the L-type Ca2+ current and a larger transient decrease of the Na+-Ca2+ exchange current on repolarization. These are attributed to decreased systolic release of Ca2+. On removal of tetracaine there was an increase of the Na+-Ca2+ exchange current. Before the addition of tetracaine, calculated Ca2+ influx and efflux across the sarcolemma were approximately equal. On adding tetracaine, efflux was transiently less than influx and, on removal of tetracaine, efflux was greater than influx. 3. These changes in Ca2+ fluxes result in an increase of cell Ca2+ during exposure to tetracaine. The calculated magnitude of this increase was equal to that measured directly by applying caffeine (20 mM) to release sarcoplasmic reticulum (SR) Ca2+ and integrating the resulting Na+-Ca2+ exchange current. 4. It is concluded that the effects of tetracaine can be accounted for by depression of calcium-induced Ca2+ release (CICR). The response is transient because the inhibition is compensated for by an increase of SR Ca2+ content such that there is no steady-state effect on the magnitude of the systolic Ca2+ transient. The consequences of this result for the effects of other modulators of CICR are discussed.
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