scholarly journals Effects of photoreleased cADP-ribose on calcium transients and calcium sparks in myocytes isolated from guinea-pig and rat ventricle

1999 ◽  
Vol 342 (2) ◽  
pp. 269-273 ◽  
Author(s):  
Yi CUI ◽  
Antony GALIONE ◽  
Derek A. TERRAR
Keyword(s):  
Guinea Pig ◽  
Mammalian Cells ◽  
Calcium Release ◽  
Ventricular Myocytes ◽  
Calcium Transients ◽  
Maximal Effect ◽  
Calcium Sparks ◽  
Whole Cell ◽  
Cell Calcium ◽  
Cardiac Ventricular Myocytes

Actions of photoreleased cADP-ribose (cADPR), a novel regulator of calcium-induced calcium release (CICR) from ryanodine-sensitive stores, were investigated in cardiac myocytes. Photoreleased cADPR caused an increase in the magnitude of whole-cell calcium transients studied in mammalian cardiac ventricular myocytes (both guinea-pig and rat) using confocal microscopy). Approx. 15 s was required following photorelease of cADPR for the development of its maximal effect. Photoreleased cADPR also increased the frequency of calcium ‘sparks’, which are thought to be elementary events which make up the whole-cell calcium transient, and were studied in rat myocytes, but had little or no effect on spark characteristics (amplitude, rise time, decay time and distance to half amplitude). The potentiating effects of photoreleased cADPR on both whole-cell transients and the frequency of calcium sparks were prevented by cytosolic application of the antagonist 8-amino-cADPR (5 μM). These experiments, therefore, provide the first evidence in any cell type for an effect of cADPR on calcium sparks, and are the first to show the actions of photoreleased cADPR on whole-cell calcium transients in mammalian cells. The observations are consistent with the effects of cADPR in enhancing the calcium sensitivity of CICR from the sarcoplasmic reticulum in cardiac ventricular myocytes, leading to an increase in the probability of occurrence of calcium sparks and to an increase in whole-cell calcium transients. The slow time-course for development of the full effect on whole-cell calcium transients might be taken to indicate that the influence of cADPR on CICR may involve complex molecular interactions rather than a simple direct action of cADPR on the ryanodine-receptor channels.

scholarly journals Whole-cell calcium current in guinea-pig ventricular myocytes dialysed with guanine nucleotides.

1990 ◽  
Vol 424 (1) ◽  
pp. 205-228 ◽  
Author(s):  
Y M Shuba ◽  
B Hesslinger ◽  
W Trautwein ◽  
T F McDonald ◽  
D Pelzer
Keyword(s):  
Guinea Pig ◽  
Calcium Current ◽  
Ventricular Myocytes ◽  
Guanine Nucleotides ◽  
Whole Cell ◽  
Cell Calcium

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 Inhibitory effect of aprindine on Na+ /Ca2+ exchange current in guinea-pig cardiac ventricular myocytes

2002 ◽  
Vol 136 (3) ◽  
pp. 361-366 ◽  
Author(s):  
Yasuhide Watanabe ◽  
Takahiro Iwamoto ◽  
Munekazu Shigekawa ◽  
Junko Kimura
Keyword(s):  
Guinea Pig ◽  
Ventricular Myocytes ◽  
Inhibitory Effect ◽  
Exchange Current ◽  
Cardiac Ventricular Myocytes

scholarly journals Inhibitory Effect of Cibenzoline on Na+/Ca2+ Exchange Current in Guinea-Pig Cardiac Ventricular Myocytes

2012 ◽  
Vol 120 (1) ◽  
pp. 59-62 ◽  
Author(s):  
Tomomi Yamakawa ◽  
Yasuhide Watanabe ◽  
Hiroshi Watanabe ◽  
Junko Kimura
Keyword(s):  
Guinea Pig ◽  
Ventricular Myocytes ◽  
Inhibitory Effect ◽  
Exchange Current ◽  
Cardiac Ventricular Myocytes

L-type Ca2+ current in guinea pig ventricular myocytes treated with modulators of tyrosine phosphorylation

1999 ◽  
Vol 276 (5) ◽  
pp. H1724-H1733 ◽  
Author(s):  
Toshitsugu Ogura ◽  
Lesya M. Shuba ◽  
Terence F. McDonald
Keyword(s):  
Guinea Pig ◽  
Tyrosine Kinase ◽  
Tyrosine Phosphorylation ◽  
Time Course ◽  
Ventricular Myocytes ◽  
Phosphotyrosine Phosphatase ◽  
Whole Cell ◽  
Phosphatase System ◽  
Tk Inhibitors ◽  
Voltage Relationship

Guinea pig ventricular myocytes in whole cell configuration were treated with tyrosine kinase (TK) inhibitors [genistein (Gst), tyrphostin A23 (T23), and tyrphostin A25 (T25)] and with inactive analogs [daidzein, genistin, and tyrphostin A1 (T1)] to measure effects on L-type Ca2+ current ( I Ca,L). Gst inhibited I Ca,L(IC50 = 47 μM) without affecting its time course or shifting the I Ca,L-voltage relationship. At the highest concentration of isoflavone tested (200 μM), I Ca,L was inhibited by 66 ± 7% (Gst), 22 ± 2% (daidzein), and 1 ± 3% (genistin). Inhibition of I Ca,L by the active tyrphostins was significantly larger than inhibition by T1; at 200 μM the inhibitions were 72 ± 6% (T23), 71 ± 6% (T25), and 27 ± 6% (T1). The phosphotyrosine phosphatase inhibitor orthovanadate (1 mM) had a small stimulatory effect (6 ± 2%) on basal I Ca,L and blocked the inhibition of I Ca,L by TK inhibitors. The data suggest a role for the TK-phosphotyrosine phosphatase system in the regulation of cardiac Ca2+ channels.

scholarly journals Calcium homeostasis in a local/global whole cell model of permeabilized ventricular myocytes with a Langevin description of stochastic calcium release

2015 ◽  
Vol 308 (5) ◽  
pp. H510-H523 ◽  
Author(s):  
Xiao Wang ◽  
Seth H. Weinberg ◽  
Yan Hao ◽  
Eric A. Sobie ◽  
Gregory D. Smith
Keyword(s):  
Calcium Release ◽  
Ventricular Myocytes ◽  
Cell Model ◽  
Ryanodine Receptors ◽  
Planck Equation ◽  
Linear Increase ◽  
Langevin Equations ◽  
Cell Models ◽  
Whole Cell ◽  
Alternative Approach

Population density approaches to modeling local control of Ca2+-induced Ca2+ release in cardiac myocytes can be used to construct minimal whole cell models that accurately represent heterogeneous local Ca2+ signals. Unfortunately, the computational complexity of such “local/global” whole cell models scales with the number of Ca2+ release unit (CaRU) states, which is a rapidly increasing function of the number of ryanodine receptors (RyRs) per CaRU. Here we present an alternative approach based on a Langevin description of the collective gating of RyRs coupled by local Ca2+ concentration ([Ca2+]). The computational efficiency of this approach no longer depends on the number of RyRs per CaRU. When the RyR model is minimal, Langevin equations may be replaced by a single Fokker-Planck equation, yielding an extremely compact and efficient local/global whole cell model that reproduces and helps interpret recent experiments that investigate Ca2+ homeostasis in permeabilized ventricular myocytes. Our calculations show that elevated myoplasmic [Ca2+] promotes elevated network sarcoplasmic reticulum (SR) [Ca2+] via SR Ca2+-ATPase-mediated Ca2+ uptake. However, elevated myoplasmic [Ca2+] may also activate RyRs and promote stochastic SR Ca2+ release, which can in turn decrease SR [Ca2+]. Increasing myoplasmic [Ca2+] results in an exponential increase in spark-mediated release and a linear increase in nonspark-mediated release, consistent with recent experiments. The model exhibits two steady-state release fluxes for the same network SR [Ca2+] depending on whether myoplasmic [Ca2+] is low or high. In the later case, spontaneous release decreases SR [Ca2+] in a manner that maintains robust Ca2+ sparks.

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