scholarly journals High [Na+]i in cardiomyocytes from rainbow trout

2007 ◽  
Vol 293 (2) ◽  
pp. R861-R866 ◽  
Author(s):  
Rikke Birkedal ◽  
Holly A. Shiels
Keyword(s):  
Rainbow Trout ◽  
Ventricular Myocytes ◽  
Resting Cells ◽  
Excitation Contraction Coupling ◽  
Contraction Coupling ◽  
Contraction Frequency ◽  
Reverse Mode ◽  
Whole Cell Patch Clamp ◽  
Ventricular Cells

Intracellular Na+-concentration, [Na+]i modulates excitation-contraction coupling of cardiac myocytes via the Na+/Ca2+ exchanger (NCX). In cardiomyocytes from rainbow trout ( Oncorhyncus mykiss), whole cell patch-clamp studies have shown that Ca2+ influx via reverse-mode NCX contributes significantly to contraction when [Na+]i is 16 mM but not 10 mM. However, physiological [Na+]i has never been measured. We recorded [Na+]i using the fluorescent indicator sodium-binding benzofuran isophthalate in freshly isolated atrial and ventricular myocytes from rainbow trout. We examined [Na+]i at rest and during increases in contraction frequency across three temperatures that span those trout experience in nature (7, 14, and 21°C). Surprisingly, we found that [Na+]i was not different between atrial and ventricular cells. Furthermore, acute temperature changes did not affect [Na+]i in resting cells. Thus, we report a resting in vivo [Na+]i of 13.4 mM for rainbow trout cardiomyocytes. [Na+]i increased from rest with increases in contraction frequency by 3.2, 4.7, and 6.5% at 0.2, 0.5, and 0.8 Hz, respectively. This corresponds to an increase of 0.4, 0.6, and 0.9 mM at 0.2, 0.5, and 0.8 Hz, respectively. Acute temperature change did not significantly affect the contraction-induced increase in [Na+]i. Our results provide the first measurement of [Na+]i in rainbow trout cardiomyocytes. This surprisingly high [Na+]i is likely to result in physiologically significant Ca2+ influx via reverse-mode NCX during excitation-contraction coupling. We calculate that this Ca2+-source will decrease with the action potential duration as temperature and contraction frequency increases.

Excitation–contraction coupling in isolated adult ventricular myocytes from the rat, dog, and rabbit: effects of various inotropic interventions in the presence of ryanodine

1986 ◽  
Vol 64 (12) ◽  
pp. 1473-1483 ◽  
Author(s):  
Magda Horackova
Keyword(s):  
Sarcoplasmic Reticulum ◽  
Ventricular Myocytes ◽  
Inotropic Agents ◽  
Inhibitory Effects ◽  
Pharmacological Interventions ◽  
Excitation Contraction Coupling ◽  
Contraction Coupling ◽  
Ventricular Cells ◽  
Contractile Activation ◽  
Dog Myocytes

Enzymatically isolated ventricular cells from rats, dogs, and rabbits were electrically stimulated and their membrane potentials were recorded simultaneously with their contractions. Specific pharmacological interventions were used to assess the relative roles of transsarcolemmal Ca2+ entry and the Ca2+ release by the sarcoplasmic reticulum in activating contractions, in these myocytes. We used ryanodine and caffeine to influence Ca2+ release by the sarcoplasmic reticulum, BAY K 8644 and epinephrine to increase Ca2+ entry through Ca2+ channels, and veratridine, ouabain, and monensin to increase Ca2+ entry through Na+–Ca2+ exchange. Ryanodine (1 μM) completely inhibited the shortenings in rat and dog myocytes, but the contractions in rabbit myocytes were much less sensitive to this alkaloid. Similar inhibitory effects of ryanodine were observed in the presence of various inotropic agents with two exceptions: caffeine's effect on the dog myocytes was relatively insensitive to ryanodine and the long-lasting tonic contractions that veratridine triggered in the myocytes of all three species remained completely unaffected by ryanodine. The data indicate that contractile activation in rat and dog ventricular cells is strongly dependent on Ca2+ release from the sarcoplasmic reticulum, while contractility in rabbit myocytes seems to be more dependent on Ca2+ entry through the sarcolemma. The ryanodine-resistant tonic contractions triggered in the myocytes of all three species in the presence of veratridine may be activated by an increased Ca2+ entry via Na+–Ca2+ exchange.

Abstract 198: Stim/orai Channel Complex In Normal And Hypertrophied Adult Cardiac Myocytes

2013 ◽  
Vol 113 (suppl_1) ◽  
Author(s):  
Jean-sebastien Hulot ◽  
Youakim Saliba ◽  
Jeremy Fauconnier ◽  
Mathilde Keck ◽  
Ludovic Bénard ◽  
...  
Keyword(s):  
Cardiac Myocytes ◽  
Ventricular Myocytes ◽  
Calcium Entry ◽  
Critical Element ◽  
Patch Clamp Technique ◽  
Excitation Contraction Coupling ◽  
Contraction Coupling ◽  
Whole Cell Patch Clamp ◽  
Adult Cardiac Myocytes ◽  
Store Operated Calcium Entry

Cardiac myocytes use Ca2+ not only in excitation-contraction coupling but also as a signaling molecule for cardiac growth. It is however unclear how Ca2+ triggers signaling in cardiac myocytes in the presence of the rapid and large Ca2+ fluctuations that occur during excitation-contraction coupling. We have recently reported that stromal interaction molecule 1 (STIM1), a calcium sensor in the sarcoplasmic reticulum, is a critical element in promoting cardiomyocyte growth through the control of a previously unrecognized sarcolemmal voltage-independent current. Our goal was to characterize the plasma membrane partners that contribute to STIM1-dependent currents in normal and hypertrophied adult cardiac myocytes. We firstly characterized the expression profile of TRPCs and ORAIs proteins in both normal and hypertrophied ventricular myocytes from abdominal aortic banded rats. The expression of TRPC1, 3, 4, 5 and 6 and of ORAI1 - 3 was identified with an up-regulation of TRPC1 in hypertrophied cells. We then used a non-viral method to deliver cy3-tagged siRNAs to ventricular myocytes to knock-down the candidate channels. The cardiac myocytes were isolated and whole cell patch-clamp technique as well as Fura-2 imaging were performed to measure the currents in cy3-labelled and in control cardiac myocytes. Our data demonstrated that the drug-inducible STIM1-dependent store-operated calcium entry was marginal in normal myocytes but was enhanced in hypertrophied myocytes. In addition, a basal inwardly rectifying current was observed in hypertrophied but not in control myocytes. This spontaneous current was recorded in the absence of calcium store depletion, required STIM1 expression and meets the characteristics of Arachidonate-Regulated Calcium selective (ARC) channels. ORAI silencing completely inhibited both store-dependent and store-independent currents suggesting the critical implication of ORAIs whereas TRPCs were only marginally involved. In conclusion, ORAI channels are involved in STIM1-dependent currents observed in hypertrophied adult cardiac myocytes. In addition to store-operated calcium entry, the STIM1/ORAI complex provides an alternative, store-independent pathway for agonist-activated Ca2+ entry.

scholarly journals Effects of mitochondrial uncoupling on Ca2+ signaling during excitation-contraction coupling in atrial myocytes

2013 ◽  
Vol 304 (7) ◽  
pp. H983-H993 ◽  
Author(s):  
Aleksey V. Zima ◽  
Malikarjuna R. Pabbidi ◽  
Stephen L. Lipsius ◽  
Lothar A. Blatter
Keyword(s):  
Ion Homeostasis ◽  
Inhibitory Effect ◽  
Partial Recovery ◽  
Atrial Myocytes ◽  
Mitochondrial Uncoupling ◽  
Release Channel ◽  
Excitation Contraction Coupling ◽  
Atp Production ◽  
Contraction Coupling ◽  
Reverse Mode

Mitochondria play an important role in intracellular Ca2+ concentration ([Ca2+]i) regulation in the heart. We studied sarcoplasmic reticulum (SR) Ca2+ release in cat atrial myocytes during depolarization of mitochondrial membrane potential (ΔΨm) induced by the protonophore FCCP. FCCP caused an initial decrease of action potential-induced Ca2+ transient amplitude and frequency of spontaneous Ca2+ waves followed by partial recovery despite partially depleted SR Ca2+ stores. In the presence of oligomycin, FCCP only exerted a stimulatory effect on Ca2+ transients and Ca2+ wave frequency, suggesting that the inhibitory effect of FCCP was mediated by ATP consumption through reverse-mode operation of mitochondrial F1F0-ATPase. ΔΨm depolarization was accompanied by cytosolic acidification, increases of diastolic [Ca2+]i, intracellular Na+ concentration ([Na+]i), and intracellular Mg2+ concentration ([Mg2+]i), and a decrease of intracellular ATP concentration ([ATP]i); however, glycolytic ATP production partially compensated for the exhaustion of mitochondrial ATP supplies. In conclusion, the initial inhibition of Ca2+ transients and waves resulted from suppression of ryanodine receptor SR Ca2+ release channel activity by a decrease in [ATP], an increase of [Mg2+]i, and cytoplasmic acidification. The later stimulation resulted from reduced mitochondrial Ca2+ buffering and cytosolic Na+ and Ca2+ accumulation, leading to enhanced Ca2+-induced Ca2+ release and spontaneous Ca2+ release in the form of Ca2+ waves. ΔΨm depolarization and the ensuing consequences of mitochondrial uncoupling observed here (intracellular acidification, decrease of [ATP]i, increase of [Na+]i and [Mg2+]i, and Ca2+ overload) are hallmarks of ischemia. These findings may therefore provide insight into the consequences of mitochondrial uncoupling for ion homeostasis, SR Ca2+ release, and excitation-contraction coupling in ischemia at the cellular and subcellular level.

Temperature-dependent expression of sarcolemmal K+ currents in rainbow trout atrial and ventricular myocytes

2002 ◽  
Vol 282 (4) ◽  
pp. R1191-R1199 ◽  
Author(s):  
Matti Vornanen ◽  
Ari Ryökkynen ◽  
Antti Nurmi
Keyword(s):  
Rainbow Trout ◽  
Cardiac Myocytes ◽  
Molecular Mechanisms ◽  
Ventricular Myocytes ◽  
Cardiac Contractility ◽  
Temperature Acclimation ◽  
Delayed Rectifier ◽  
Rainbow Trout Oncorhynchus Mykiss ◽  
Delayed Rectifier Current ◽  
Ventricular Cells

Temperature has a strong influence on the excitability and the contractility of the ectothermic heart that can be alleviated in some species by temperature acclimation. The molecular mechanisms involved in the temperature-induced improvement of cardiac contractility and excitability are, however, still poorly known. The present study examines the role of sarcolemmal K+ currents from rainbow trout ( Oncorhynchus mykiss) cardiac myocytes after thermal acclimation. The two major K+ conductances of the rainbow trout cardiac myocytes were identified as the Ba2+-sensitive background inward rectifier current ( I K1) and the E-4031-sensitive delayed rectifier current ( I Kr). In atrial cells, the density of I K1 is very low and the density of I Kr is remarkably high. The opposite is true for ventricular cells. Acclimation to cold (4°C) modified the two K+ currents in opposite ways. Acclimation to cold increases the density of I Kr and depresses the density of I K1. These changes in repolarizing K+ currents alter the shape of the action potential, which is much shorter in cold-acclimated than warm-acclimated (17°C) trout. These results provide the first concrete evidence that K+channels of trout cardiac myocytes are adaptable units that provide means to regulate cardiac excitability and contractility as a function of temperature.

scholarly journals Models of cardiac excitation–contraction coupling in ventricular myocytes

2010 ◽  
Vol 226 (1) ◽  
pp. 1-15 ◽  
Author(s):  
George S.B. Williams ◽  
Gregory D. Smith ◽  
Eric A. Sobie ◽  
M. Saleet Jafri
Keyword(s):  
Ventricular Myocytes ◽  
Excitation Contraction Coupling ◽  
Contraction Coupling ◽  
Cardiac Excitation

Biphasic effects of cell volume on excitation-contraction coupling in rabbit ventricular myocytes

2002 ◽  
Vol 282 (4) ◽  
pp. H1270-H1277 ◽  
Author(s):  
Gui-Rong Li ◽  
Min Zhang ◽  
Leslie S. Satin ◽  
Clive M. Baumgarten
Keyword(s):  
Action Potential ◽  
Cell Volume ◽  
Action Potential Duration ◽  
Ventricular Myocytes ◽  
Current Clamp ◽  
Osmotic Swelling ◽  
Excitation Contraction Coupling ◽  
Contraction Coupling ◽  
Fura 2 ◽  
Rabbit Ventricular Myocytes

We studied the effects of osmotic swelling on the components of excitation-contraction coupling in ventricular myocytes. Myocyte volume rapidly increased 30% in hyposmotic (0.6T) solution and was constant thereafter. Cell shortening transiently increased 31% after 4 min in 0.6T but then decreased to 68% of control after 20 min. In parallel, the L-type Ca2+ current ( I Ca-L) transiently increased 10% and then declined to 70% of control. Similar biphasic effects on shortening were observed under current clamp. In contrast, action potential duration was unchanged at 4 min but decreased to 72% of control after 20 min. Ca2+ transients were measured with fura 2-AM. The emission ratio with excitation at 340 and 380 nm (f340/f380) decreased by 12% after 3 min in 0.6T, whereas shortening and I Ca-L increased at the same time. After 8 min, shortening, I Ca-L, and the f340/f380 ratio decreased 28, 25, and 59%, respectively. The results suggest that osmotic swelling causes biphasic changes in I Ca-L that contribute to its biphasic effects on contraction. In addition, swelling initially appears to reduce the Ca2+ transient initiated by a given I Ca-L, and later, both I Ca-L and the Ca2+ transient are inhibited.

Sign in / Sign up

Export Citation Format

Share Document