scholarly journals Effects of high extracellular [K+] and adrenaline on force development, relaxation and membrane potential in cardiac muscle from freshwater turtle and rainbow trout

2001 ◽  
Vol 204 (2) ◽  
pp. 261-268 ◽  
Author(s):  
J.S. Nielsen ◽  
H. Gesser
Keyword(s):  
Rainbow Trout ◽  
Sarcoplasmic Reticulum ◽  
Action Potential ◽  
Freshwater Turtle ◽  
Force Amplitude ◽  
Excitation Contraction Coupling ◽  
Twitch Force ◽  
Contraction Coupling ◽  
High K ◽  
Low K

Increases in extracellular K(+) concentrations reduced the twitch force amplitude of heart muscle from the freshwater turtle (Trachemys scripta elegans) and rainbow trout (Oncorhynchus mykiss). Adrenaline augmented twitch force amplitude and reduced the relative influence of [K(+)]. In the absence of adrenaline, high [K(+)] had less effect in reducing twitch force in turtle than in trout, whereas the reverse was true in the presence of adrenaline. Under anoxic conditions, twitch force was lower in 10 mmol l(−1) than in 2.5 mmol l(−1) K(+) in both preparations, but adrenaline removed this difference. A further analysis of turtle myocardium showed that action potential duration was shorter and resting potential more positive in high [K(+)] than in low [K(+)]. Adrenaline restored the duration of the action potential, but did not affect the depolarisation, which may attenuate Na(+)/Ca(2+) exchange, participating in excitation/contraction coupling. The contractile responses in the presence of adrenaline were, however, similar in both high and low K(+) concentrations when increases in extracellular Ca(2+) were applied to increase the demand on excitation/contraction coupling. The possibilities that adrenaline counteracts the effects of high [K(+)] via the sarcoplasmic reticulum or sarcolemmal Na(+)/K(+)-ATPase were examined by inhibiting the sarcoplasmic reticulum with ryanodine (10 micromol l(−1)) or Na(+)/K(+)-ATPase with ouabain (0.25 or 3 mmol l(−)). No evidence to support either of these possibilities was found. Adrenaline did not protect all aspects of excitation/contraction coupling because the maximal frequency giving regular twitches was lower at 10 mmol l(−1) K(+) than at 2.5 mmol l(−1) K(+).

Junctional Sarcoplasmic Reticulum in Excitation-Contraction-Coupling

1982 ◽  
Vol 40 ◽  
pp. 136-137
Author(s):  
J.R. Sommer ◽  
E. Bossen ◽  
A. Fabiato
Keyword(s):  
Sarcoplasmic Reticulum ◽  
Action Potential ◽  
Muscle Contraction ◽  
Cardiac Cells ◽  
Close Apposition ◽  
Excitation Contraction Coupling ◽  
Contraction Coupling ◽  
Terminal Cisterna ◽  
Voltage Dependent ◽  
Junctional Sarcoplasmic Reticulum

The junctional sarcoplasmic reticulum (JSR, syn. terminal cisterna) is implicated in Ca++storage and release for muscle contraction. Its discrete ultrastructure permits distinction from the rest of the SR (free SR) even when it occurs without plasmalemmal contact, e.g. as extended JSR (EJSR) in bird, and corbular SR (CSR) in mammalian cardiac cells. The close apposition of JSR to plasmalemma via junctional processes is central to proposed mechanisms of translating voltage-dependent charge transfers at the plasmalemma during the action potential into Ca++release from the JSR. These hypotheses are put into question by the existence of EJSR (and CSR) which in birds constitutes 70-80% of the total JSR. An alternate hypothesis proposes, at least for cardiac cells, that Ca++entering the cell during excitation causes additional Ca++to be freed intracellularly. The notion of a chemical transmitter acting by diffusion is attractive because it will allow for the anomalous topography of EJSR, especially since bird cardiac cells have only about half the diameter of their mammalian relatives and have no transverse tubules.

Voltage Sensors and Calcium Channels of Excitation-Contraction Coupling

Physiology ◽  
1988 ◽  
Vol 3 (6) ◽  
pp. 223-227 ◽  
Author(s):  
E Rios ◽  
G Pizarro
Keyword(s):  
Skeletal Muscle ◽  
Sarcoplasmic Reticulum ◽  
Calcium Channels ◽  
Action Potential ◽  
Structural Data ◽  
Excitation Contraction Coupling ◽  
Voltage Sensors ◽  
Contraction Coupling ◽  
Chemical Mediation ◽  
Mechanical Connection

Three mechanisms are proposed for the transduction from action potential to Ca2+ release from the sarcoplasmic reticulum in skeletal muscle: Chemical mediation, a mechanical connection between transverse tubular membrane and sacroplasmic reticulum, and Ca2+-induced release of Ca2+. New biochemical, biophysical, and structural data favor a mechanical connection and add the possibility that Ca2+-induced Ca2+-release is working in parallel.

Overexpression of human β2-adrenergic receptors increases gain of excitation-contraction coupling in mouse ventricular myocytes

2004 ◽  
Vol 287 (3) ◽  
pp. H1029-H1038 ◽  
Author(s):  
Scott A. Grandy ◽  
Eileen M. Denovan-Wright ◽  
Gregory R. Ferrier ◽  
Susan E. Howlett
Keyword(s):  
Sarcoplasmic Reticulum ◽  
Action Potential ◽  
Adrenergic Receptors ◽  
Action Potentials ◽  
Ventricular Myocytes ◽  
Wild Type ◽  
Excitation Contraction Coupling ◽  
Contraction Coupling ◽  
Cardiac Excitation ◽  
Action Potential Configuration

This study investigated cardiac excitation-contraction coupling at 37°C in transgenic mice with cardiac-specific overexpression of human β2-adrenergic receptors (TG4 mice). In field-stimulated myocytes, contraction was significantly greater in TG4 compared with wild-type (WT) ventricular myocytes. In contrast, when duration of depolarization was controlled with rectangular voltage clamp steps, contraction amplitudes initiated by test steps were the same in WT and TG4 myocytes. When cells were voltage clamped with action potentials simulating TG4 and WT action potential configurations, contractions were greater with long TG4 action potentials and smaller with shorter WT action potentials, which suggests an important role for action potential configuration. Interestingly, peak amplitude of L-type Ca2+ current ( ICa-L) initiated by rectangular test steps was reduced, although the voltage dependencies of contractions and currents were not altered. To explore the basis for the altered relation between contraction and ICa-L, Ca2+ concentrations were measured in myocytes loaded with fura 2. Diastolic concentrations of free Ca2+ and amplitudes of Ca2+ transients were similar in voltage-clamped myocytes from WT and TG4 mice. However, sarcoplasmic reticulum (SR) Ca2+ content assessed with the rapid application of caffeine was elevated in TG4 cells. Increased SR Ca2+ was accompanied by increased frequency and amplitudes of spontaneous Ca2+ sparks measured at 37°C with fluo 3. These observations suggest that the gain of Ca2+-induced Ca2+ release is increased in TG4 myocytes. Increased gain counteracts the effects of decreased amplitude of ICa-L in voltage-clamped myocytes and likely contributes to increased contraction amplitudes in field-stimulated TG4 myocytes.

The Effect of Lanthanum on Excitation–Contraction Coupling in Frog Skeletal Muscle

1974 ◽  
Vol 52 (6) ◽  
pp. 1126-1135 ◽  
Author(s):  
D. J. Parry ◽  
A. Kover ◽  
G. B. Frank
Keyword(s):  
Skeletal Muscle ◽  
Action Potential ◽  
Muscle Membrane ◽  
Frog Skeletal Muscle ◽  
Tension Development ◽  
Excitation Contraction Coupling ◽  
Contraction Coupling ◽  
Reduced Rate ◽  
Caffeine Contractures

Exposure of frog toe muscles to 1 mM La3+ results in a decrease in amplitude and rate of tension development of potassium contractures and twitches. At this concentration La3+ also inhibits the uptake of calcium, both in the resting condition and during stimulation. Caffeine contractures are unaffected even after a 5-min pre-exposure to La3+. The depolarization induced by various concentrations of K+ is reduced by about 10 mV as is the amplitude of the action potential. The rate of rise of the action potential is reduced by about 40% after 1 min in La3+ Ringer. Neither the decreased amplitude nor the reduced rate of depolarization is considered to be sufficient to explain the inhibition of tension development. It is suggested that La3+ partially uncouples excitation from contraction by preventing the release of a trigger-Ca2+ fraction from some site on the muscle membrane. This fraction normally plays a role in excitation–contraction coupling, although some tension may still be developed in the absence of a trigger-Ca2+ influx.

Effect of Several Cations on Transmembrane Potentials of Cardiac Muscle

1956 ◽  
Vol 186 (2) ◽  
pp. 317-324 ◽  
Author(s):  
Brian F. Hoffman ◽  
E. E. Suckling
Keyword(s):  
Action Potential ◽  
Cardiac Muscle ◽  
Action Potentials ◽  
Time Course ◽  
Pacemaker Activity ◽  
Transmembrane Potentials ◽  
High K ◽  
Intracellular Microelectrodes ◽  
Simultaneous Decrease ◽  
Low K

The effects of changes in the extracellular concentrations of Ca, K and Mg on the transmembrane resting and action potentials of single fibers of the auricle, ventricle and specialized conducting system of the dog heart have been studied by means of intracellular microelectrodes. With respect to Ca, the three tissues exhibit quite different sensitivities. Changes in concentration of this ion alter the time course of the action potential recorded from auricle and ventricle but have little effect on the action potential configuration of the Purkinje fiber. In the latter tissue, on the other hand, pacemaker activity is most strongly enhanced by Ca depletion and excitability is lost at Ca concentrations permitting normal propagation in papillary muscle. The effect of K on the resting transmembrane potential is dependent on the simultaneous Ca concentration. The interrelationship is such that the depolarizing effect of high K is decreased by elevated Ca and the depolarization produced by low K is diminished by low levels of Ca. Changes in the concentration of Mg have little effect on the transmembrane potentials of cardiac muscle unless the level of Ca is low. Under this condition a simultaneous decrease in Mg gives rise to a marked prolongation of the action potential duration of both auricle and ventricle. Some evidence for the basic similarity of the processes underlying repolarization in these three tissues is presented and it is thought the normally encountered differences in their action potentials may be related to the sensitivity of each tissue to extracellular Ca.

Sarcoplasmic reticulum, potassium, and cardiac force in rainbow trout and plaice

1989 ◽  
Vol 257 (3) ◽  
pp. R599-R604 ◽  
Author(s):  
M. F. el-Sayed ◽  
H. Gesser
Keyword(s):  
Steady State ◽  
Rainbow Trout ◽  
Sarcoplasmic Reticulum ◽  
Similar Increase ◽  
Stimulation Rate ◽  
Twitch Force ◽  
Force Development ◽  
Rest Periods ◽  
Ventricular Tissue

The role played by the sarcoplasmic reticulum in force development and in cellular Ca2+ balance and its dependence on extracellular K+ were examined in heart ventricular tissue of rainbow trout and plaice. Compared with the steady-state twitch at a stimulation rate of 0.2 Hz, a 30-s rest led to a similar increase in twitch force in trout heart, regardless of whether [K+] was 2.5 or 5 mM. At 5 mM (but not at 2.5 mM) post-rest potentiation increased with increasing rest periods (from 30 to 900 s). These post-rest potentiations were removed or transformed into a loss of force by 10 microM ryanodine or 8 mM caffeine. In the plaice heart, where the sarcoplasmic reticulum is claimed to be sparse, the post-rest potentiation and the influence of ryanodine were small. The Ca2+ uptake measured during 5 min with 45Ca in the trout heart was higher in 5 than in 2.5 mM K+, regardless of the concomitant stimulation rate. This effect of K+ was removed by 10 microM ryanodine. The twitch force after 5 min of rest correlated significantly with the Ca2+ uptake, whereas the twitch force developed at a rate of 0.2 or 1.0 Hz did not. In conclusion, an elevation of K+ appears to stimulate the Ca2+ uptake of the sarcoplasmic reticulum. The twitch force after prolonged rest seems to relate to the Ca2+ contained in this organelle, whereas this does not apply to the twitch force developed at more physiological rates (0.2 or 1 Hz).

Calmodulin and Excitation-Contraction Coupling

Physiology ◽  
2000 ◽  
Vol 15 (6) ◽  
pp. 281-284 ◽  
Author(s):  
Susan L. Hamilton ◽  
Irina Serysheva ◽  
Gale M. Strasburg
Keyword(s):  
Skeletal Muscle ◽  
Ion Channels ◽  
Sarcoplasmic Reticulum ◽  
Release Channel ◽  
Excitation Contraction Coupling ◽  
Transverse Tubule ◽  
Contraction Coupling ◽  
Voltage Dependent ◽  
Important Regulator ◽  
Precise Role

Excitation-contraction coupling in cardiac and skeletal muscle involves the transverse-tubule voltage-dependent Ca2+ channel and the sarcoplasmic reticulum Ca2+ release channel. Both of these ion channels bind and are modulated by calmodulin in both its Ca2+-bound and Ca2+-free forms. Calmodulin is, therefore, potentially an important regulator of excitation-contraction coupling. Its precise role, however, has not yet been defined.

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