scholarly journals Retraction: Calmodulin kinase and a calmodulin-binding 'IQ' domain facilitate L-type Ca2+current in rabbit ventricular myocytes by a common mechanism

2015 ◽  
Vol 593 (9) ◽  
pp. 2249-2249
Keyword(s):  
Ventricular Myocytes ◽  
Common Mechanism ◽  
Calmodulin Binding ◽  
Calmodulin Kinase ◽  
Rabbit Ventricular Myocytes

scholarly journals C Terminus L‐type Ca 2+ Channel Calmodulin‐Binding Domains are ‘Auto‐Agonist’ Ligands in Rabbit Ventricular Myocytes

2003 ◽  
Vol 550 (3) ◽  
pp. 731-738 ◽  
Author(s):  
Igor Dzhura ◽  
Yuejin Wu ◽  
Rong Zhang ◽  
Roger J. Colbran ◽  
Susan L. Hamilton ◽  
...  
Keyword(s):  
Ventricular Myocytes ◽  
Calmodulin Binding ◽  
Binding Domains ◽  
C Terminus ◽  
Rabbit Ventricular Myocytes ◽  
Agonist Ligands

Abstract 3503: Hydrogen Peroxide-Induced Afterdepolarizations are Dependent on Calmodulin Kinase II Signaling

Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Lai-Hua Xie ◽  
Fuhua Chen ◽  
James N Weiss
Keyword(s):  
Oxidative Stress ◽  
Hydrogen Peroxide ◽  
Ventricular Myocytes ◽  
Heart Association ◽  
Early Afterdepolarizations ◽  
Calmodulin Kinase ◽  
Repolarization Reserve ◽  
Delayed Afterdepolarizations ◽  
Rabbit Ventricular Myocytes ◽  
Camkii Activation

Background: In the heart, hydrogen peroxide (H 2 O 2 ) has been shown to cause early afterdepolarizations (EADs) and triggered activity by impairing Na current (I Na ) inactivation. Since H 2 O 2 has been recently shown to activate Ca 2+ /calmodulin kinase II (CaMKII), and since CaMKII activation has also been reported to impair I Na inactivation and predispose to EADs, we hypothesized that CaMKII activation by H 2 O 2 may be an important factor in the genesis of EADs induced by oxidative stress. Methods and Results: Patch-clamped Fluo-4 AM-loaded rabbit ventricular myocytes were exposed to H 2 O 2 (0.1–1mM), which induced spontaneous EADs after 5–15 min. Both the I Na blocker tetrodoxtin (TTX, 10 μM) and the I Ca,L blocker nifedipine shortened AP duration (APD) and suppressed EADs. H 2 O 2 increased both peak and steady-state I Ca,L under square-pulse voltage clamp, and enhanced I Ca,L to a greater extent during the AP plateau than during the AP upstroke under AP clamp conditions. In addition, by prolonging the AP plateau and increasing Ca influx via maintained I Ca,L , H 2 O 2 -induced EADs frequently caused DADs delayed afterdepolarizations (DADs) due to spontaneous SR Ca release waves after repolarization. KN-93(1 μM), a CaMKII inhibitor, prevented H 2 O 2 -induced EADs (n=4), whereas the inactive analogue KN-92 did not (n=5). Conclusion: These findings indicate that H 2 O 2 -induced EADs depend on both impaired I Na inactivation to reduce repolarization reserve and enhanced I Ca,L to reverse repolarization. Intact CaMKII signaling is necessary for EAD generation in this setting, presumably via its actions on I Na and I Ca,L , although direct redox effects on other ion channels/transporters may also be important. Our observations support a link between increased oxidative stress, CaMKII activation and afterdepolarizations as triggers of lethal ventricular arrhythmias in diseased heart. This research has received full or partial funding support from the American Heart Association, AHA National Center.

scholarly journals Regulation of Sarcoplasmic Reticulum [Ca2+] during Rest in Rabbit Ventricular Myocytes

2011 ◽  
Vol 100 (3) ◽  
pp. 560a
Author(s):  
Elisa Bovo ◽  
Aleksey V. Zima
Keyword(s):  
Sarcoplasmic Reticulum ◽  
Ventricular Myocytes ◽  
Rabbit Ventricular Myocytes

Effects of Volatile Anesthetic Isoflurane on ATP-Sensitive K+Channels in Rabbit Ventricular Myocytes

1996 ◽  
Vol 229 (3) ◽  
pp. 852-856 ◽  
Author(s):  
Jin Han ◽  
Euiyong Kim ◽  
Won Kyung Ho ◽  
Yung E. Earm
Keyword(s):  
Ventricular Myocytes ◽  
Volatile Anesthetic ◽  
K Channels ◽  
Rabbit Ventricular Myocytes

scholarly journals Caveolae in Rabbit Ventricular Myocytes: Distribution and Dynamic Diminution after Cell Isolation

2017 ◽  
Vol 113 (5) ◽  
pp. 1047-1059 ◽  
Author(s):  
Rebecca A.B. Burton ◽  
Eva A. Rog-Zielinska ◽  
Alexander D. Corbett ◽  
Rémi Peyronnet ◽  
Ilona Bodi ◽  
...  
Keyword(s):  
Ventricular Myocytes ◽  
Cell Isolation ◽  
Rabbit Ventricular Myocytes

Steady-state twitch Ca2+ fluxes and cytosolic Ca2+ buffering in rabbit ventricular myocytes

1996 ◽  
Vol 270 (1) ◽  
pp. C192-C199 ◽  
Author(s):  
L. M. Delbridge ◽  
J. W. Bassani ◽  
D. M. Bers
Keyword(s):  
Steady State ◽  
Sarcoplasmic Reticulum ◽  
Voltage Clamp ◽  
Ventricular Myocytes ◽  
Cell Voltage ◽  
Whole Cell ◽  
Rabbit Ventricular Myocytes ◽  
The Mean ◽  
State Contraction ◽  
Caffeine Contractures

Intracellular Ca2+ ([Ca2+]i) transients and transsarcolemmal Ca2+ currents were measured in indo 1-loaded isolated rabbit ventricular myocytes during whole cell voltage clamp to quantitate the components of cytosolic Ca2+ influx and to describe the dynamic aspects of cytosolic Ca2+ buffering during steady-state contraction (0.5 Hz, 22 degrees C). Sarcolemmal Ca2+ influx was directly measured from the integrated Ca2+ current (Ica) recorded during the clamp (158 +/- 10 attomoles; amol). Sarcoplasmic reticulum (SR) Ca2+ content was determined from the integrated electrogenic Na+/Ca2+ exchange current (Ix) induced during rapid application and sustained exposure of cells to caffeine to elicit the release of the SR Ca2+ load (1,208 +/- 170 amol). The mean steady-state SR Ca2+ load was calculated to be 87 +/- 13 microM (mumol/l nonmitochondrial cytosolic volume). Ca2+ influx via Ica represented approximately 14% of the stored SR Ca2+ and 23% of the total cytosolic Ca2+ flux during a twitch (47 +/- 6 microM). Comparison of electrophysiologically measured Ca2+ fluxes with Ca2+ transients yields apparent buffering values of 60 for caffeine contractures and 110 for twitches (delta Ca2+ total/delta Ca2+ free). This is consistent with the occurrence of "active" buffering of cytosolic Ca2+ by SR Ca2+ uptake during the twitch.

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