Regulation of contraction and relaxation by membrane  potential in cardiac ventricular myocytes

Ferrier, Gregory R.; Redondo, Isabel M.; Mason, Cindy A.; Mapplebeck, Cindy; Howlett, Susan E.

doi:10.1152/ajpheart.2000.278.5.h1618

Cited by 20 publications

(26 citation statements)

References 37 publications

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“…L-type channel, in molluscs as in lower vertebrates, is thought to be the primary pathway for Ca 2? entry for the excitation-contraction mechanism (Ferrier et al 2000;Bers andPerez-Reyes 1999, Ö dblom et al 2000).…”

Section: Discussionmentioning

confidence: 99%

Establishment of functional primary cultures of heart cells from the clam Ruditapes decussatus

Hanana¹,

Talarmin²,

Pennec³

et al. 2011

Cytotechnology

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Heart cells from the clam Ruditapes decussatus were routinely cultured with a high level of reproducibility in sea water based medium. Three cell types attached to the plastic after 2 days and could be maintained in vitro for at least 1 month: epithelial-like cells, round cells and fibroblastic cells. Fibroblastic cells were identified as functional cardiomyocytes due to their spontaneous beating, their ultrastructural characteristics and their reactivity with antibodies against sarcomeric a-actinin, sarcomeric tropomyosin, myosin and troponin T-C. Patch clamp measurements allowed the identification of ionic currents characteristic of cardiomyocytes: a delayed potassium current (I K slow ) strongly suppressed (95%) by tetraethylammonium (1 mM), a fast inactivating potassium current (I K fast ) inhibited (50%) by 4 amino-pyridine at 1 mM and, at a lower level (34%) by TEA, a calcium dependent potassium current (I KCa ) activated by strong depolarization. Three inward voltage activated currents were also characterized in some cardiomyocytes: L-type calcium current (I Ca ) inhibited by verapamil at 5 9 10 -4 M, T-type Ca 2? current, rapidly activated and inactivated, and sodium current (I Na ) observed in only a few cells after strong hyperpolarization. These two currents did not seem to be physiologically essential in the initiation of the beatings of cardiomyocytes. Potassium currents were partially inhibited by tributyltin (TBT) (1 lM) but not by okadaic acid (two marine pollutants). DNA synthesis was also demonstrated in few cultured cells using BrdU (bromo-2 0 -deoxyuridine). Observed effects of okadaic acid and TBT demonstrated that cultured heart cells from clam Ruditapes decussatus can be used as an experimental model in marine toxicology.

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Section: Discussionmentioning

confidence: 99%

Establishment of functional primary cultures of heart cells from the clam Ruditapes decussatus

Hanana¹,

Talarmin²,

Pennec³

et al. 2011

Cytotechnology

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“…There is direct evidence that forced repolarization by an electric stimulus causes relaxation (7,10) and deactivates Ca 2ϩ transients (7). Ferrier et al (7) measured cell shortening in guinea pig ventricular cells after forced repolarization and discovered that the cells immediately relaxed and intracellular Ca 2ϩ concentration immediately decreased after the repolarizing stimulus.…”

Section: Discussionmentioning

confidence: 99%

Left ventricular geometry immediately following defibrillation: shock-induced relaxation

Jongh

Ramanathan

Hoffmeister

et al. 2003

American Journal of Physiology-Heart and Circulatory Physiology

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. Left ventricular geometry immediately following defibrillation: shock-induced relaxation. Am J Physiol Heart Circ Physiol 284: H815-H819, 2003. First published October 31, 2002 10.1152/ajpheart.00093.2002 ultrasound study suggested that there is relaxation of the myocardium after defibrillation. The 2D study could not measure activity occurring within the first 33 ms after the shock, a period that may be critical for discriminating between shock-and excitation-induced relaxation. The objective of our study was to determine the left ventricular (LV) geometry during the first 33 ms after defibrillation. Biphasic defibrillation shocks were delivered 5-50 s after the induction of ventricular fibrillation in each of the seven dogs. One-dimensional, short-axis ultrasound images of the LV cavity were acquired at a rate of 250 samples/s. The LV cavity diameter was computed from 32 ms before to 32 ms after the shock. Preshock and postshock percent changes in LV diameter were analyzed as a function of time with the use of regression analysis. The normalized mean pre-and postshock slopes (0.2 Ϯ 2.2 and 3.3 Ϯ 7.9% per 10 ms) were significantly different (P Ͻ 0.01). The postshock slope was positive (P Ͻ 0.005). Our results confirm that the bulk of the myocardium is relaxing immediately after defibrillation. deexcitation; ultrasound; cardiac mechanics MUCH RESEARCH has concentrated on determining the electrical phenomenon that can predict either the success or failure of ventricular defibrillation. Many studies suggest that excitation (depolarization) of the myocardium plays an important role in defibrillation (2,13,14,16,18) by extinguishing fibrillatory wave fronts [critical mass theory (18)] or by preventing any new fibrillatory wave fronts from forming after the defibrillation shock (2). However, recent studies (4, 11) suggest that deexcitation (repolarization) may be an important factor in determining the success or failure of defibrillation.Measurements have been made in isolated heart preparations to support deexcitation as a key mechanism for defibrillation. Efimov et al. (4) measured action potentials on the epicardium of isolated rabbit hearts after a defibrillation shock and observed that deexcitation is induced in part of the epicardial surface. The limitation of this previous study is that it is in vitro and only measures the electrical activity on the heart surface: it does not provide information on the electrical state of the bulk of the myocardium. Entcheva et al. (6) have shown that the transmembrane potential measured on the epicardium can be very different from that measured in the midmyocardium and that in vitro potentials can vary significantly from in vivo. Thus deexcitation has yet to be confirmed in the bulk of the myocardium or in vivo.A study by Malkin et al. (11) measured left ventricular (LV) geometry in canines after defibrillation by using two-dimensional (2D) ultrasound imaging. Their study was the first to measure the mechanical activity in the myocardium after a defibrillation shock. The 2...

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“…Extracellular [Ca 2ϩ ] was rapidly changed from 2.0 mM to 0.1, 0.5, or 5.0 mM by bathing the cell in buffers of different [Ca 2ϩ ]. A computer-controlled rapid solution changer was used to rapidly expose the cell to solutions with different [Ca 2ϩ ] for 3 s following the conditioning pulse train and throughout the test step (17). In some experiments, the extracellular Mg 2ϩ concentration also was elevated from 1 to 4 mM.…”

Section: Myocyte Isolationmentioning

confidence: 99%

Increases in diastolic [Ca²⁺] can contribute to positive inotropy in guinea pig ventricular myocytes in the absence of changes in amplitudes of Ca²⁺ transients

Shutt

Ferrier²,

Howlett³

2006

American Journal of Physiology-Heart and Circulatory Physiology

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Increases in contraction amplitude following rest or in elevated extracellular Ca(2+) concentration ([Ca(2+)]) have been attributed to increased sarcoplasmic reticulum (SR) Ca(2+) stores and/or increased trigger Ca(2+). However, either manipulation also may elevate diastolic [Ca(2+)]. The objective of this study was to determine whether elevation of diastolic [Ca(2+)] could contribute to positive inotropy in isolated ventricular myocytes. Voltage-clamp experiments were conducted with high-resistance microelectrodes in isolated myocytes at 37 degrees C. Intracellular free [Ca(2+)] was measured with fura-2, and cell shortening was measured with an edge detector. SR Ca(2+) stores were assessed with 10 mM caffeine (0 mM Na(+), 0 mM Ca(2+)). Following a period of rest, cells were activated with trains of pulses, which generated contractions of increasing amplitude, called positive staircases. Positive staircases were accompanied by increasing diastolic [Ca(2+)] but no change in Ca(2+) transient amplitudes. When extracellular [Ca(2+)] was elevated from 2.0 to 5.0 mM, resting intracellular [Ca(2+)] increased and resting cell length decreased. Amplitudes of contractions and L-type Ca(2+) current increased in elevated extracellular [Ca(2+)], although SR Ca(2+) stores, assessed by rapid application of caffeine, did not increase. Although Ca(2+) transient amplitude did not increase in 5.0 mM extracellular [Ca(2+)], diastolic [Ca(2+)] continued to increase with increasing extracellular [Ca(2+)]. These data suggest that increased diastolic [Ca(2+)] contributes to positive inotropy following rest or with increasing extracellular [Ca(2+)] in guinea pig ventricular myocytes.

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Regulation of contraction and relaxation by membrane potential in cardiac ventricular myocytes

Cited by 20 publications

References 37 publications

Establishment of functional primary cultures of heart cells from the clam Ruditapes decussatus

Establishment of functional primary cultures of heart cells from the clam Ruditapes decussatus

Left ventricular geometry immediately following defibrillation: shock-induced relaxation

Increases in diastolic [Ca²⁺] can contribute to positive inotropy in guinea pig ventricular myocytes in the absence of changes in amplitudes of Ca²⁺ transients

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Regulation of contraction and relaxation by membrane potential in cardiac ventricular myocytes

Cited by 20 publications

References 37 publications

Establishment of functional primary cultures of heart cells from the clam Ruditapes decussatus

Establishment of functional primary cultures of heart cells from the clam Ruditapes decussatus

Left ventricular geometry immediately following defibrillation: shock-induced relaxation

Increases in diastolic [Ca2+] can contribute to positive inotropy in guinea pig ventricular myocytes in the absence of changes in amplitudes of Ca2+ transients

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Increases in diastolic [Ca²⁺] can contribute to positive inotropy in guinea pig ventricular myocytes in the absence of changes in amplitudes of Ca²⁺ transients