An estimate of the calcium content of the sarcoplasmic reticulum in rat ventricular myocytes

Varró, Andrea; Negretti, Nicholas M.; Hester, S. B.; Eisner, David

doi:10.1007/bf00374975

Cited by 202 publications

(184 citation statements)

References 6 publications

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“…Consistent with previous reports, cell capacitance was significantly lower in atrophic than in control cardiac myocytes (123±3 pF, n=96 vs. 161±5 pF, n=98, p<0.0001) [40]. At a holding potential of V Pip =−90 mV, Ca 2+ release from the SR was induced by rapid superperfusion of the investigated cardiac myocyte with 10 mmol/l caffeine [30,38,49,50,54]. In the presence of caffeine, Ca 2+ is released from the SR, cannot be stored in the SR again and is therefore completely removed from the cytoplasm by the Na + -Ca 2+ exchanger [8,27].…”

Section: Sr Ca 2+ Contentsupporting

confidence: 90%

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Enhanced Ca2+ influx through cardiac L-type Ca2+ channels maintains the systolic Ca2+ transient in early cardiac atrophy induced by mechanical unloading

Biermann¹,

Bernhardt²,

Neef³

et al. 2014

Thorac cardiovasc Surg

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Cardiac atrophy as a consequence of mechanical unloading develops following exposure to microgravity or prolonged bed rest. It also plays a central role in the reverse remodelling induced by left ventricular unloading in patients with heart failure. Surprisingly, the intracellular Ca 2+ transients which are pivotal to electromechanical coupling and to cardiac plasticity were repeatedly found to remain unaffected in early cardiac atrophy. To elucidate the mechanisms underlying the preservation of the Ca 2+ transients, we investigated Ca 2+ cycling in cardiomyocytes from mechanically unloaded (heterotopic abdominal heart transplantation) and control (orthotopic) hearts in syngeneic Lewis rats. Following 2 weeks of unloading, sarcoplasmic reticulum (SR) Ca 2+ content was reduced by~55 %. Atrophic cardiac myocytes also showed a much lower frequency of spontaneous diastolic Ca 2+ sparks and a diminished systolic Ca 2+ release, even though the expression of ryanodine receptors was increased by~30 %. In contrast, current clamp recordings revealed prolonged action potentials in endocardial as well as epicardial myocytes which were associated with a two to fourfold higher sarcolemmal Ca 2+ influx under action potential clamp. In addition, Cav1.2 subunits which form the pore of L-type

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Section: Sr Ca 2+ Contentsupporting

confidence: 90%

“…2b). More importantly, the integral of I ti (Q caff ), which reflects the total amount of Ca 2+ released from the SR [49], was significantly smaller (~−55 %) in the atrophic cardiac myocytes (Fig. 2c).…”

Section: Sr Ca 2+ Contentmentioning

confidence: 96%

Enhanced Ca2+ influx through cardiac L-type Ca2+ channels maintains the systolic Ca2+ transient in early cardiac atrophy induced by mechanical unloading

Biermann¹,

Bernhardt²,

Neef³

et al. 2014

Thorac cardiovasc Surg

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“…To test this, we measured SR Ca 2ϩ by using the integral of the NCX current produced by application of 10 mmol/L caffeine. 27 In the example shown in Figure 3A, caffeine (0.5 mmol/L) did not produce waves. The addition of isoproterenol (in the presence of caffeine) increased SR Ca 2ϩ content and initiated Ca 2ϩ waves.…”

Section: Resultsmentioning

confidence: 89%

Increasing Ryanodine Receptor Open Probability Alone Does Not Produce Arrhythmogenic Calcium Waves

Venetucci

Trafford

Eisner

2007

Circulation Research

176

151

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Abstract-Diastolic waves of Ca 2ϩ release have been shown to activate delayed afterdepolarizations as well as some cardiac arrhythmias. The aim of this study was to investigate whether increasing ryanodine receptor open probability alone or in the presence of ␤-adrenergic stimulation produces diastolic Ca release from the sarcoplasmic reticulum (SR). When voltage-clamped rat ventricular myocytes were exposed to caffeine (0.5 to 1.0 mmol), diastolic Ca 2ϩ release was seen to accompany the first few stimuli but was never observed in the steady state. We attribute the initial phase of diastolic Ca 2ϩ release to a decrease in the threshold SR Ca 2ϩ content required to activate Ca 2ϩ waves and its subsequent disappearance to a decrease of SR content below this threshold. Application of isoproterenol (1 mol

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“…The SR Ca 2ϩ content was measured by integrating a 20 mmol/L caffeine-induced transient inward current. 9,10 Ethical approval was obtained by the Royal Brompton and Harefield NHS Trust Ethics Committee. Informed consent was obtained from each patient.…”

Section: Methodsmentioning

confidence: 99%

Clinical Recovery From End-Stage Heart Failure Using Left-Ventricular Assist Device and Pharmacological Therapy Correlates With Increased Sarcoplasmic Reticulum Calcium Content but Not With Regression of Cellular Hypertrophy

et al. 2004

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Background-Left ventricular assist device (LVAD) treatment is known to lead to structural and functional cellular modifications in the heart. The relevance of these changes for clinical recovery is unknown. Methods and Results-We compared properties of cardiomyocytes obtained from tissue taken at explantation of the LVAD in patients with clinical recovery with those obtained from hearts of patients who did not show clinical recovery, thus requiring transplantation. Compared with myocytes taken at implantation, both the recovery and nonrecovery groups showed Ϸ50% reduction in cell capacitance, an index of cell size. However, action potential duration shortened, L-type Ca 2ϩ current fast inactivation was more rapid, and sarcoplasmic reticulum Ca 2ϩ content was increased in the recovery compared with the nonrecovery group. Conclusions-These results show that specific changes in excitation-contraction coupling, and not regression of cellular hypertrophy, are specifically associated with clinical recovery after LVAD and further identify sarcoplasmic reticulum Ca Key Words: mechanical devices Ⅲ electrophysiology Ⅲ heart failure Ⅲ myocytes Ⅲ sarcoplasmic reticulum H eart transplantation is currently the only effective longterm treatment for patients in end-stage heart failure. Recently, left ventricular assist device (LVAD) treatment has been used successfully as a bridge to transplantation, as destination therapy in patients with contraindications to transplantation, 1 or to obtain recovery in a small number of patients. 2,3 We have shown that in some patients with idiopathic dilated cardiomyopathy in end-stage heart failure, combined LVAD and pharmacological therapy induced clinical recovery to allow explantation of the device without recurrence of heart failure. 3 LVAD treatment results in numerous changes in cardiomyocyte phenotype, excitation-contraction coupling, gene expression, and function. 2 Whether these changes are beneficial is not known. Regression of hypertrophy is thought to be an important factor in recovery. 2 However, several studies have also shown that hypertrophy is not required as a compensatory response to pressure overload, 4 and its regression is not necessarily associated with normalization of electrophysiological parameters. 5 Cardiomyocytes isolated from biopsies taken at explantation of the LVAD in patients with clinical recovery showed reductions in cell volume and cell surface area. L-type Ca 2ϩ current and sarcoplasmic reticulum (SR) Ca 2ϩ content were increased in myocytes during recovery, suggesting a critical role for intracellular Ca 2ϩ homeostasis. 6 Increased SR Ca 2ϩ uptake in cardiac tissue after LVAD treatment has also been described previously. 7 However, whether these specific cellular changes are related to clinical recovery remained unclear.In this study, we compared findings in cardiomyocytes obtained from tissue taken from patients who recovered with those obtained from patients who, despite identical treatment, did not. This allowed correlation between cellular electroph...

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An estimate of the calcium content of the sarcoplasmic reticulum in rat ventricular myocytes

Cited by 202 publications

References 6 publications

Enhanced Ca2+ influx through cardiac L-type Ca2+ channels maintains the systolic Ca2+ transient in early cardiac atrophy induced by mechanical unloading

Enhanced Ca2+ influx through cardiac L-type Ca2+ channels maintains the systolic Ca2+ transient in early cardiac atrophy induced by mechanical unloading

Increasing Ryanodine Receptor Open Probability Alone Does Not Produce Arrhythmogenic Calcium Waves

Clinical Recovery From End-Stage Heart Failure Using Left-Ventricular Assist Device and Pharmacological Therapy Correlates With Increased Sarcoplasmic Reticulum Calcium Content but Not With Regression of Cellular Hypertrophy

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