The role of intracellular Ca buffers in determining the shape of the systolic Ca transient in cardiac ventricular myocytes

2001 ◽  
Vol 442 (1) ◽  
pp. 96-100 ◽  
Author(s):  
M.E. Díaz ◽  
A.W. Trafford ◽  
D.A. Eisner
Keyword(s):  
Ventricular Myocytes ◽  
Intracellular Ca ◽  
Cardiac Ventricular Myocytes

scholarly journals Dual role of junctin in the regulation of ryanodine receptors and calcium release in cardiac ventricular myocytes

2011 ◽  
Vol 589 (24) ◽  
pp. 6063-6080 ◽  
Author(s):  
Beth A. Altschafl ◽  
Demetrios A. Arvanitis ◽  
Oscar Fuentes ◽  
Qunying Yuan ◽  
Evangelia G. Kranias ◽  
...  
Keyword(s):  
Calcium Release ◽  
Ventricular Myocytes ◽  
Ryanodine Receptors ◽  
Dual Role ◽  
Cardiac Ventricular Myocytes

scholarly journals The calcium stored in the sarcoplasmic reticulum acts as a safety mechanism in rainbow trout heart

2014 ◽  
Vol 307 (12) ◽  
pp. R1493-R1501 ◽  
Author(s):  
Caroline Cros ◽  
Laurent Sallé ◽  
Daniel E. Warren ◽  
Holly A. Shiels ◽  
Fabien Brette
Keyword(s):  
Rainbow Trout ◽  
Sarcoplasmic Reticulum ◽  
Ventricular Myocytes ◽  
Adrenergic Stimulation ◽  
Relative Contribution ◽  
Safety Mechanism ◽  
Rapid Changes ◽  
Intracellular Ca ◽  
As Stress

Cardiomyocyte contraction depends on rapid changes in intracellular Ca2+. In mammals, Ca2+ influx as L-type Ca2+ current ( ICa) triggers the release of Ca2+ from sarcoplasmic reticulum (SR) and Ca2+-induced Ca2+ release (CICR) is critical for excitation-contraction coupling. In fish, the relative contribution of external and internal Ca2+ is unclear. Here, we characterized the role of ICa to trigger SR Ca2+ release in rainbow trout ventricular myocytes using ICa regulation by Ca2+ as an index of CICR. ICa was recorded with a slow (EGTA) or fast (BAPTA) Ca2+ chelator in control and isoproterenol conditions. In the absence of β-adrenergic stimulation, the rate of ICa inactivation was not significantly different in EGTA and BAPTA (27.1 ± 1.8 vs. 30.3 ± 2.4 ms), whereas with isoproterenol (1 μM), inactivation was significantly faster with EGTA (11.6 ± 1.7 vs. 27.3 ± 1.6 ms). When barium was the charge carrier, inactivation was significantly slower in both conditions (61.9 ± 6.1 vs. 68.0 ± 8.7 ms, control, isoproterenol). Quantification revealed that without isoproterenol, only 39% of ICa inactivation was due to Ca2+, while with isoproterenol, inactivation was Ca2+-dependent (∼65%) and highly reliant on SR Ca2+ (∼46%). Thus, SR Ca2+ is not released in basal conditions, and ICa is the main trigger of contraction, whereas during a stress response, SR Ca2+ is an important source of cytosolic Ca2+. This was not attributed to differences in SR Ca2+ load because caffeine-induced transients were not different in both conditions. Therefore, Ca2+ stored in SR of trout cardiomyocytes may act as a safety mechanism, allowing greater contraction when higher contractility is required, such as stress or exercise.

CaM kinase augments cardiac L-type Ca2+ current: a cellular mechanism for long Q-T arrhythmias

1999 ◽  
Vol 276 (6) ◽  
pp. H2168-H2178 ◽  
Author(s):  
Yuejin Wu ◽  
Leigh B. MacMillan ◽  
R. Blair McNeill ◽  
Roger J. Colbran ◽  
Mark E. Anderson
Keyword(s):  
Ventricular Myocytes ◽  
Ryanodine Receptors ◽  
Cam Kinase ◽  
Early Afterdepolarizations ◽  
Ultrastructural Studies ◽  
Intracellular Ca ◽  
Dependent Protein ◽  
T Tubules ◽  
Rabbit Ventricular Myocytes

Early afterdepolarizations (EAD) caused by L-type Ca2+ current ( I Ca,L) are thought to initiate long Q-T arrhythmias, but the role of intracellular Ca2+ in these arrhythmias is controversial. Rabbit ventricular myocytes were stimulated with a prolonged EAD-containing action potential-clamp waveform to investigate the role of Ca2+/calmodulin-dependent protein kinase II (CaM kinase) in I Ca,L during repolarization. I Ca,L was initially augmented, and augmentation was dependent on Ca2+ from the sarcoplasmic reticulum because the augmentation was prevented by ryanodine or thapsigargin. I Ca,Laugmentation was also dependent on CaM kinase, because it was prevented by dialysis with the inhibitor peptide AC3-I and reconstituted by exogenous constitutively active CaM kinase when Ba2+ was substituted for bath Ca2+. Ultrastructural studies confirmed that endogenous CaM kinase, L-type Ca2+ channels, and ryanodine receptors colocalized near T tubules. EAD induction was significantly reduced in current-clamped cells dialyzed with AC3-I (4/15) compared with cells dialyzed with an inactive control peptide (11/15, P = 0.013). These findings support the hypothesis that EADs are facilitated by CaM kinase.

The functional role of cardiac T-tubules explored in a model of rat ventricular myocytes

2006 ◽  
Vol 364 (1842) ◽  
pp. 1187-1206 ◽  
Author(s):  
Michal Pásek ◽  
Jiři Šimurda ◽  
Georges Christé
Keyword(s):  
Ventricular Myocytes ◽  
Contractile Activity ◽  
Tubular Lumen ◽  
Current Clamp Mode ◽  
Intracellular Ca ◽  
Ionic Changes ◽  
Access Resistance ◽  
T Tubules ◽  
Tubular Membranes

The morphology of the cardiac transverse-axial tubular system (TATS) has been known for decades, but its function has received little attention. To explore the possible role of this system in the physiological modulation of electrical and contractile activity, we have developed a mathematical model of rat ventricular cardiomyocytes in which the TATS is described as a single compartment. The geometrical characteristics of the TATS, the biophysical characteristics of ion transporters and their distribution between surface and tubular membranes were based on available experimental data. Biophysically realistic values of mean access resistance to the tubular lumen and time constants for ion exchange with the bulk extracellular solution were included. The fraction of membrane in the TATS was set to 56%. The action potentials initiated in current-clamp mode are accompanied by transient K + accumulation and transient Ca 2+ depletion in the TATS lumen. The amplitude of these changes relative to external ion concentrations was studied at steady-state stimulation frequencies of 1–5 Hz. Ca 2+ depletion increased from 7 to 13.1% with stimulation frequency, while K + accumulation decreased from 4.1 to 2.7%. These ionic changes (particularly Ca 2+ depletion) implicated significant decrease of intracellular Ca 2+ load at frequencies natural for rat heart.

Antisense inhibition of Na+/Ca2+ exchange during anoxia/reoxygenation in ventricular myocytes

2001 ◽  
Vol 281 (5) ◽  
pp. H2184-H2190 ◽  
Author(s):  
B. N. Eigel ◽  
R. W. Hadley
Keyword(s):  
Guinea Pig ◽  
Antisense Oligonucleotide ◽  
Ventricular Myocytes ◽  
Antisense Inhibition ◽  
Start Site ◽  
Intracellular Ca

This study investigated the role of the Na+/Ca2+ exchanger (NCX) in regulating cytosolic intracellular Ca2+concentration ([Ca2+]i) during anoxia/reoxygenation in guinea pig ventricular myocytes. The hypothesis that the NCX is the predominant mechanism mediating [Ca2+]i overload in this model was tested through inhibition of NCX expression by an antisense oligonucleotide. Immunocytochemistry revealed that this antisense oligonucleotide, directed at the area around the start site of the guinea pig NCX1, specifically reduced NCX expression in cultured adult myocytes by 90 ± 4%. Antisense treatment inhibited evoked NCX activity by 94 ± 3% and decreased the rise in [Ca2+]i during anoxia/reoxygenation by 95 ± 3%. These data suggest that NCX is the predominant mechanism mediating Ca2+ overload during anoxia/reoxygenation in guinea-pig ventricular myocytes.

scholarly journals From syncitium to regulated pump: a cardiac muscle cellular update

2011 ◽  
Vol 35 (1) ◽  
pp. 22-27 ◽  
Author(s):  
Donna H. Korzick
Keyword(s):  
Cardiac Muscle ◽  
Intracellular Signaling ◽  
Ventricular Myocytes ◽  
Cellular Events ◽  
Intracellular Ca ◽  
Health And Disease ◽  
Cardiac Excitation ◽  
And Function ◽  
Cardiac Automaticity

The primary purpose of this article is to present a basic overview of some key teaching concepts that should be considered for inclusion in an six- to eight-lecture introductory block on the regulation of cardiac performance for graduate students. Within the context of cardiac excitation-contraction coupling, this review incorporates information on Ca2+ microdomains and local control theory, with particular emphasis on the role of Ca2+ sparks as a key regulatory component of ventricular myocyte contraction dynamics. Recent information pertaining to local Ca2+ cycling in sinoatrial nodal cells (SANCs) as a mechanism underlying cardiac automaticity is also presented as part of the recently described coupled-clock pacemaker system. The details of this regulation are emerging; however, the notion that the sequestration and release of Ca2+ from internal stores in SANCs (similar to that observed in ventricular myocytes) regulates the rhythmic excitation of the heart (i.e., membrane ion channels) is an important advancement in this area. The regulatory role of cardiac adrenergic receptors on cardiac rate and function is also included, and fundamental concepts related to intracellular signaling are discussed. An important point of emphasis is that whole organ cardiac dynamics can be traced back to cellular events regulating intracellular Ca2+ homeostasis and, as such, provides an important conceptual framework from which students can begin to think about whole organ physiology in health and disease. Greater synchrony of Ca2+-regulatory mechanisms between ventricular and pacemaker cells should enhance student comprehension of complex regulatory phenomenon in cardiac muscle.

Dual roles of mitochondrial KATP channels in diazoxide-mediated protection in isolated rabbit hearts

2001 ◽  
Vol 280 (1) ◽  
pp. H246-H255 ◽  
Author(s):  
Sheng Wang ◽  
James Cone ◽  
Yongge Liu
Keyword(s):  
Ventricular Myocytes ◽  
Critical Time ◽  
Katp Channels ◽  
Channel Blockers ◽  
Dual Roles ◽  
Channel Opening ◽  
Mitochondrial Redox State ◽  
Intracellular Ca ◽  
Mitochondrial Katp Channels

Whether the mitochondrial ATP-dependent potassium (mKATP) channel is the trigger or the mediator of cardioprotection is controversial. We investigated the critical time sequences of mKATP channel opening for cardioprotection in isolated rabbit hearts. Pretreatment with diazoxide (100 μM), a selective mKATP channel opener, for 5 min followed by 10 min washout before the 30-min ischemia and 2-h reperfusion significantly reduced infarct size (9 ± 3 vs. 35 ± 3% in control), indicating a role of mKATP channels as a trigger of protection. The protection was blocked by coadministration of the L-type Ca2+ channel blockers nifedipine (100 nM) or 5-hydroxydecanoic acid (5-HD; 50 μM) or by the protein kinase C (PKC) inhibitor chelerythrine (5 μM). The protection of diazoxide was not blocked by 50 μM 5-HD but was blocked by 200 μM 5-HD or 10 μM glybenclamide administrated 5 min before and throughout the 30 min of ischemia, indicating a role of mKATP opening as a mediator of protection. Giving diazoxide throughout the 30 min of ischemia also protected the heart, and the protection was not blocked by chelerythrine. Nifedipine did not affect the ability of diazoxide to open mKATP channels assessed by mitochondrial redox state. In electrically stimulated rabbit ventricular myocytes, diazoxide significantly increased Ca2+ transient but had no effect on L-type Ca2+ currents. Our results suggest that opening of mKATP channels can trigger cardioprotection. The trigger phase may be induced by elevation of intracellular Ca2+ and activation of PKC. During the lethal ischemia, mKATPchannel opening mediates the protection, independent of PKC, by yet unknown mechanisms.

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