A mechanism distinct from the L-type Ca current or Na–Ca exchange contributes to Ca entry in rat ventricular myocytes

Kupittayanant, P.; Trafford, Andrew W.; Díaz, M. E.; Eisner, David

doi:10.1016/j.ceca.2006.01.011

Cited by 19 publications

(21 citation statements)

References 23 publications

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“…Because mechanically induced Ca 2± entry into cardiomyocytes could occur via other channels or transporters,20,21 we assessed possible roles of trans-sarcolemmal Ca 2± influx using the half-cell stretch protocol in Na ± /Ca 2± -free solution (0NC; containing [in mmol/L] LiCl 140, KCl 10, EGTA 10, MgCl 2 1, HEPES 5, glucose 11). The perfusate was switched from normal Tyrode to 0NC 5 seconds before stretch application to record control spark rate.…”

Section: Resultsmentioning

confidence: 99%

Axial Stretch of Rat Single Ventricular Cardiomyocytes Causes an Acute and Transient Increase in Ca ²⁺ Spark Rate

Iribe

Ward

Camelliti

et al. 2009

Circulation Research

179

180

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We investigate acute effects of axial stretch, applied by carbon fibers (CFs), on diastolic Ca2± spark rate in rat isolated cardiomyocytes. CFs were attached either to both cell ends (to maximize the stretched region), or to the center and one end of the cell (to compare responses in stretched and nonstretched half-cells). Sarcomere length was increased by 8.01 ± 0.94% in the stretched cell fraction, and time series of XY confocal images were recorded to monitor diastolic Ca2± spark frequency and dynamics. Whole-cell stretch causes an acute increase of Ca2± spark rate (to 130.7 ± 6.4%) within 5 seconds, followed by a return to near background levels (to 104.4±5.1%) within 1 minute of sustained distension. Spark rate increased only in the stretched cell region, without significant differences in spark amplitude, time to peak, and decay time constants of sparks in stretched and nonstretched areas. Block of stretch-activated ion channels (2 gmol/L GsMTx-4), perfusion with Na±/Ca2±-free solution, and block of nitric oxide synthesis (1 mmol/L L-NAME) all had no effect on the stretch-induced acute increase in Ca2± spark rate. Conversely, interference with cytoskeletal integrity (2 hours of 10 gmol/L colchicine) abolished the response. Subsequent electron microscopic tomography confirmed the close approximation of microtubules with the T-tubular–sarcoplasmic reticulum complex (to within · 10−8m). In conclusion, axial stretch of rat cardiomyocytes acutely and transiently increases sarcoplasmic reticulum Ca2± spark rate via a mechanism that is independent of sarcolemmal stretch-activated ion channels, nitric oxide synthesis, or availability of extracellular calcium but that requires cytoskeletal integrity. The potential of microtubule-mediated modulation of ryanodine receptor function warrants further investigation.

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Section: Resultsmentioning

confidence: 99%

Axial Stretch of Rat Single Ventricular Cardiomyocytes Causes an Acute and Transient Increase in Ca ²⁺ Spark Rate

Iribe

Ward

Camelliti

et al. 2009

Circulation Research

179

180

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“…Thus as the L‐type current disappears this remaining efflux must be required to balance some other source of influx that under these conditions constitutes the total Ca 2+ influx. The identity of this background influx is unknown (see Kupittayanant et al 2006 for further discussion).…”

Section: Discussionmentioning

confidence: 99%

The effects of membrane potential, SR Ca²⁺ content and RyR responsiveness on systolic Ca²⁺ alternans in rat ventricular myocytes

Díaz

Eisner

et al. 2009

The Journal of Physiology

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Previous work has shown that small depolarizing pulses produce a beat to beat alternation in the amplitude of the systolic Ca 2+ transient in ventricular myocytes. The aim of the present work was to investigate the role of changes of SR Ca 2+ content and L-type Ca 2+ current in this alternans. As the amplitude of the depolarizing pulse was increased from 10 to 30 mV the magnitude of alternans decreased. Confocal linescan studies showed that this was accompanied by an increase in the number of sites from which Ca 2+ waves propagated. A sudden decrease in the depolarisation amplitude resulted in three classes of behaviour: (1)

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“…When both the L-type Ca channel and NCX were inhibited, this background entry mechanism was revealed by the decrease of [Ca 2+ ] i on maintained depolarization, an effect attributed to a decreased driving force. 168 A major limitation of the analysis was the lack of a specific inhibitor with only gadolinium having a marked effect.…”

Section: Resting Camentioning

confidence: 99%

Calcium and Excitation-Contraction Coupling in the Heart

Eisner

Caldwell

Kistamás

et al. 2017

Circulation Research

597

460

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Cardiac contractility is regulated by changes in intracellular Ca concentration ([Ca2+]i). Normal function requires that [Ca2+]i be sufficiently high in systole and low in diastole. Much of the Ca needed for contraction comes from the sarcoplasmic reticulum and is released by the process of calcium-induced calcium release. The factors that regulate and fine-tune the initiation and termination of release are reviewed. The precise control of intracellular Ca cycling depends on the relationships between the various channels and pumps that are involved. We consider 2 aspects: (1) structural coupling: the transporters are organized within the dyad, linking the transverse tubule and sarcoplasmic reticulum and ensuring close proximity of Ca entry to sites of release. (2) Functional coupling: where the fluxes across all membranes must be balanced such that, in the steady state, Ca influx equals Ca efflux on every beat. The remainder of the review considers specific aspects of Ca signaling, including the role of Ca buffers, mitochondria, Ca leak, and regulation of diastolic [Ca2+]i.

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A mechanism distinct from the L-type Ca current or Na–Ca exchange contributes to Ca entry in rat ventricular myocytes

Cited by 19 publications

References 23 publications

Axial Stretch of Rat Single Ventricular Cardiomyocytes Causes an Acute and Transient Increase in Ca ²⁺ Spark Rate

Axial Stretch of Rat Single Ventricular Cardiomyocytes Causes an Acute and Transient Increase in Ca ²⁺ Spark Rate

The effects of membrane potential, SR Ca²⁺ content and RyR responsiveness on systolic Ca²⁺ alternans in rat ventricular myocytes

Calcium and Excitation-Contraction Coupling in the Heart

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A mechanism distinct from the L-type Ca current or Na–Ca exchange contributes to Ca entry in rat ventricular myocytes

Cited by 19 publications

References 23 publications

Axial Stretch of Rat Single Ventricular Cardiomyocytes Causes an Acute and Transient Increase in Ca 2+ Spark Rate

Axial Stretch of Rat Single Ventricular Cardiomyocytes Causes an Acute and Transient Increase in Ca 2+ Spark Rate

The effects of membrane potential, SR Ca2+ content and RyR responsiveness on systolic Ca2+ alternans in rat ventricular myocytes

Calcium and Excitation-Contraction Coupling in the Heart

Contact Info

Product

Resources

About

Axial Stretch of Rat Single Ventricular Cardiomyocytes Causes an Acute and Transient Increase in Ca ²⁺ Spark Rate

Axial Stretch of Rat Single Ventricular Cardiomyocytes Causes an Acute and Transient Increase in Ca ²⁺ Spark Rate

The effects of membrane potential, SR Ca²⁺ content and RyR responsiveness on systolic Ca²⁺ alternans in rat ventricular myocytes