ArticleThe Journal of physiology1998
Na+-Ca2+ exchange and sarcoplasmic reticular Ca2+ regulation in ventricular myocytes from transgenic mice overexpressing the Na+-Ca2+ exchanger.
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 33 papers.
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Who cites it
33 citing papers in PubMed, 147 citations in OpenAlex.
- CaCell calcium · 2020Review
- Myocardial slices come to age: an intermediate complexity in vitro cardiac model for translational research.Cardiovascular research · 2020Review
- Changes in cellular CaThe Journal of physiology · 2020Article
- Pathophysiology of Calcium Mediated Ventricular Arrhythmias and Novel Therapeutic Options with Focus on Gene Therapy.International journal of molecular sciences · 2019Review
- Loss of p21-activated kinase 1 (Pak1) promotes atrial arrhythmic activity.Heart rhythm · 2018Article
- Age- and strain-related aberrant CaAmerican journal of physiology. Heart and circulatory physiology · 2017Article
- Overexpression of junctophilin-2 does not enhance baseline function but attenuates heart failure development after cardiac stress.Proceedings of the National Academy of Sciences of the United States of America · 2014Article
- Na/Ca exchange and contraction of the heart.Journal of molecular and cellular cardiology · 2013Review
- Statistically enhanced spectral counting approach to TCDD cardiac toxicity in the adult zebrafish heart.Journal of proteome research · 2013Article
- Mechanical and energetic properties of papillary muscle from ACTC E99K transgenic mouse models of hypertrophic cardiomyopathy.American journal of physiology. Heart and circulatory physiology · 2013Article
- Therapeutic cardiac-targeted delivery of miR-1 reverses pressure overload-induced cardiac hypertrophy and attenuates pathological remodeling.Journal of the American Heart Association · 2013Article
- Induced overexpression of Na(+)/Ca(2+) exchanger does not aggravate myocardial dysfunction induced by transverse aortic constriction.Journal of cardiac failure · 2013Article
- Effects of increased systolic Ca(2+) and β-adrenergic stimulation on Ca(2+) transient decline in NOS1 knockout cardiac myocytes.Nitric oxide : biology and chemistry · 2012Article
- Reduced Na(+) and higher K(+) channel expression and function contribute to right ventricular origin of arrhythmias in Scn5a+/- mice.Open biology · 2012Article
- Proarrhythmia in a non-failing murine model of cardiac-specific Na+/Ca 2+ exchanger overexpression: whole heart and cellular mechanisms.Basic research in cardiology · 2012Article
- Constitutive overexpression of phosphomimetic phospholemman S68E mutant results in arrhythmias, early mortality, and heart failure: potential involvement of Na+/Ca2+ exchanger.American journal of physiology. Heart and circulatory physiology · 2012Article
- Cardiac electrophysiology in mice: a matter of size.Frontiers in physiology · 2012Article
- Characterization of calumenin-SERCA2 interaction in mouse cardiac sarcoplasmic reticulum.The Journal of biological chemistry · 2009Article
- Induced overexpression of Na+/Ca2+ exchanger transgene: altered myocyte contractility, [Ca2+]i transients, SR Ca2+ contents, and action potential duration.American journal of physiology. Heart and circulatory physiology · 2009Article
- Molecular cardiology in translation: gene, cell and chemical-based experimental therapeutics for the failing heart.Journal of cardiovascular translational research · 2008Review
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 2 countries.
Funding
Abstract
1. The contribution of the sarcoplasmic reticulum (SR) and Na+-Ca2+ exchanger to intracellular Ca2+ regulation in mouse cardiac myocytes was investigated by measuring contraction after variable rest intervals, rapid cooling contractures (RCCs) and fast application of caffeine. The results obtained showed differences from other species in the roles played by the SR and the Na+-Ca2+ exchanger. They suggest that in mouse ventricular myocytes there is significant Ca2+ entry via the exchanger during rest and during the latter part of the Ca2+ transient. 2. In cardiac myocytes isolated from transgenic mice overexpressing the cardiac Na+-Ca2+ exchanger the time to peak and relaxation of twitches and RCCs were faster than in control littermates. The decline of Ca2+, assessed by indo-1 fluorescence, was faster in transgenic myocytes even in the absence of Na+ and Ca2+ in the superfusing solution. This suggests that SR Ca2+ uptake is faster in these myocytes. However, no difference in the expression of SERCA2a, phospholamban or calsequestrin measured with Western blotting could be found in the two groups. 3. We measured SR Ca2+ content by integrating the caffeine-induced transient inward current. The amount of Ca2+ stored in the SR of transgenic mouse myocytes was 69 % greater than in non-transgenic littermates. The increased SR Ca2+ content may be responsible for the faster rate of SR Ca2+ release and uptake in cells from transgenic mice. 4. We performed experiments to assess whether the reversal potential of the Na+-Ca2+ exchanger (ENa-Ca) was different in transgenic cardiac cells. We measured a Ni2+-sensitive current elicited by voltage ramps in non-dialysed myocytes. The current-voltage relationship showed no difference in the reversal potential of the Na+-Ca2+ exchanger in transgenic and control myocytes. This suggests that the effects on the SR Ca2+ content in transgenic cardiac myocytes can be ascribed to the overexpression of the exchanger and are not secondary to changes in intracellular diastolic Ca2+ and Na+.
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