Excitation-Contraction Coupling: Relationship of Slow Inward Current to Contraction

1989 ◽  
pp. 227-239
Author(s):  
Terence F. McDonald
Keyword(s):  
Slow Inward Current ◽  
Excitation Contraction Coupling ◽  
Inward Current ◽  
Contraction Coupling ◽  
Coupling Relationship ◽  
Relationship Of

Participation of slow inward current in the Purkinje fiber action potential overshoot

1979 ◽  
Vol 237 (2) ◽  
pp. H204-H212
Author(s):  
L. Mary-Rabine ◽  
B. F. Hoffman ◽  
M. R. Rosen
Keyword(s):  
Action Potential ◽  
Action Potentials ◽  
Purkinje Fiber ◽  
Slow Inward Current ◽  
Inward Current ◽  
Slow Channel ◽  
Phase 0 ◽  
Relationship Of ◽  
The Relationship ◽  
Diastolic Potential

We used microelectrode techniques to study the relationship of canine Purkinje fiber membrane potential and the action potential (AP) overshoot. At the maximum diastolic potential, -93.0 +/- 0.5 (SE) mV, AP overshoot was +37.7 +/- 0.4 mV. There was a range of membrane potentials (MP) less negative than the maximum diastolic potential from which action potentials were elicited with an overshoot greater than the control. Starting at an MP of less than -78.7 +/- 0.4 mV, AP overshoot was less than control. A maximum overshoot of +40.2 +/- 0.4 mV occurred at an MP of -85.4 +/- 0.4 mV. The relationship of the maximum upstroke velocity (Vmax) of phase 0 depolarization to MP was sigmoidal. Peak Vmax, 497 +/- 13 V/s, occurred at MP greater than or equal to -89.3 +/- 0.5 mV. The increase in overshoot was enhanced as perfusate [Ca2+] increased and decreased as [Ca2+] decreased. Slow-channel blocking agents and tetrodotoxin (TTX) depressed the peak of the curve relating overshoot to MP. TTX also decreased Vmax. The effect of TTX on overshoot but not on Vmax was reversed with Ca2+, 8.1 mM. The increase in overshoot for action potentials initiated during the terminal part of phase 3 was due to a slow, delayed component of the upstroke and appears to result from the slow inward current.

scholarly journals The Voltage-sensitive Release Mechanism of Excitation Contraction Coupling in Rabbit Cardiac Muscle Is Explained by Calcium-induced Calcium Release

2003 ◽  
Vol 121 (5) ◽  
pp. 353-373 ◽  
Author(s):  
H. Griffiths ◽  
K.T. MacLeod
Keyword(s):  
Calcium Release ◽  
Outward Current ◽  
Disulfonic Acid ◽  
Release Mechanism ◽  
Tonic Component ◽  
Excitation Contraction Coupling ◽  
Inward Current ◽  
Contraction Coupling ◽  
Cell Shortening ◽  
Calcium Induced Calcium Release

The putative voltage-sensitive release mechanism (VSRM) was investigated in rabbit cardiac myocytes at 37°C with high resistance microelectrodes to minimize intracellular dialysis. When the holding potential was adjusted from −40 to −60 mV, the putative VSRM was expected to operate alongside CICR. Under these conditions however, we did not observe a plateau at positive potentials of the cell shortening versus voltage relationship. The threshold for cell shortening changed by −10 mV, but this resulted from a similar change of the threshold for activation of inward current. Cell shortening under conditions where the putative VSRM was expected to operate was blocked in a dose dependent way by nifedipine and CdCl2 and blocked completely by NiCl2. “Tail contractions” persisted in the presence of nifedipine and CdCl2 but were blocked completely by NiCl2. Block of early outward current by 4-aminopyridine and 4-acetoamido-4′-isothiocyanato-stilbene-2,2′-disulfonic acid (SITS) demonstrated persisting inward current during test depolarizations despite the presence of nifedipine and CdCl2. Inward current did not persist in the presence of NiCl2. A tonic component of cell shortening that was prominent during depolarizations to positive potentials under conditions selective for the putative VSRM was sensitive to rapidly applied changes in superfusate [Na+] and to the outward Na+/Ca2+ exchange current blocking drug KB-R7943. This component of cell shortening was thought to be the result of Na+/Ca2+ exchange–mediated excitation contraction coupling. Cell shortening recorded under conditions selective for the putative VSRM was increased by the enhanced state of phosphorylation induced by isoprenaline (1 μM) and by enhancing sarcoplasmic reticulum Ca2+ content by manipulation of the conditioning steps. Under these conditions, cell shortening at positive test depolarizations was converted from tonic to phasic. We conclude that the putative VSRM is explained by CICR with the Ca2+ “trigger” supplied by unblocked L-type Ca2+ channels and Na+/Ca2+ exchange.

Excitation–contraction coupling model to estimate the recirculating fraction of activator calcium in intact cardiac muscle

1990 ◽  
Vol 68 (8) ◽  
pp. 1041-1048 ◽  
Author(s):  
Ferdinand Urthaler ◽  
Alfred A. Walker ◽  
Russell C. Reeves ◽  
Lloyd L. Hefner
Keyword(s):  
Steady State ◽  
Coupling Model ◽  
Hill Coefficient ◽  
Slow Inward Current ◽  
Excitation Contraction Coupling ◽  
Contraction Coupling ◽  
Extracellular Compartment ◽  
Sigmoidal Curve ◽  
State Force ◽  
The Hill

Potentiated contractions were evoked with a rapid pace pause maneuver in 14 length-clamped ferret papillary muscles paced 12 times/min at 25 °C. At 1.25 mM [Ca2+]o the average steady-state force was 2.94 ± 1.08 g/mm2 and the potentiated contraction averaged 10.96 ± 1.61 g/mm2. At 5.0 mM [Ca2+]o the steady-state force increased to 6.18 ± 1.23 g/mm2 and the potentiated contraction averaged 12.08 ± 1.15 g/mm2. Under the conditions of these experiments the potentiated contraction obtained at 5.0 mM [Ca2+]o is equal to the maximum twitch tension (Fmax) these muscles can generate. We have previously shown that Fmax is an equivalent of maximal calcium activated force. Since there is a beat to beat nearly exponential decay of the evoked potentiation, the fraction (= fraction x) of the potentiation that is not dissipated with each beat is nearly constant. Using an excitation–contraction coupling model we have previously found that x reflects a measure of the recirculating fraction of activator calcium. Because the tension–calcium relationship is better characterized by a sigmoidal curve, we have now incorporated the Hill equation in the model. To account for the inverse relationship between [Ca2+]i and the magnitude of the slow inward current, a term for negative feedback (h) was also included. We have determined the quantity (x – h) because x and h could not be determined separately. The quantity (x – h) was denoted as x′. The average values of x′ at 1.25 and 5.0 mM [Ca2+]o were significantly different (p < 0.0001), approximately 20% at the lower [Ca2+]o and about 50% at the higher [Ca2+]o. An attempt to estimate both x′ and the Hill coefficient N simultaneously has shown that the determination of N must be considered inaccurate, but even larger variations of N have little influence on x′. Thus, in intact ferret ventricular muscle, the model predicts that at 1.25 mM [Ca2+]o only about 20% of the activator calcium recirculates, while some 80% comes across the sarcolemma from the extracellular compartment. The model also predicts that the recirculating fraction doubles when [Ca2+]o is elevated to 5 mM.Key words: length-clamped papillary muscle, maximum twitch tension, excitation–contraction coupling model, recirculating fraction of activator calcium, transsarcolemmal fraction of activator calcium.

scholarly journals Remodeling of t-system and proteins underlying excitation-contraction coupling in aging versus failing human heart

2021 ◽  
Vol 7 (1) ◽  
Author(s):  
Yankun Lyu ◽  
Vipin K. Verma ◽  
Younjee Lee ◽  
Iosif Taleb ◽  
Rachit Badolia ◽  
...  
Keyword(s):  
Heart Function ◽  
Ventricular Myocardium ◽  
Left Ventricular ◽  
Left Ventricular Myocardium ◽  
Excitation Contraction Coupling ◽  
Transverse Tubular System ◽  
Contraction Coupling ◽  
Senescent Phenotype ◽  
Cellular Microstructure ◽  
T System

AbstractIt is well established that the aging heart progressively remodels towards a senescent phenotype, but alterations of cellular microstructure and their differences to chronic heart failure (HF) associated remodeling remain ill-defined. Here, we show that the transverse tubular system (t-system) and proteins underlying excitation-contraction coupling in cardiomyocytes are characteristically remodeled with age. We shed light on mechanisms of this remodeling and identified similarities and differences to chronic HF. Using left ventricular myocardium from donors and HF patients with ages between 19 and 75 years, we established a library of 3D reconstructions of the t-system as well as ryanodine receptor (RyR) and junctophilin 2 (JPH2) clusters. Aging was characterized by t-system alterations and sarcolemmal dissociation of RyR clusters. This remodeling was less pronounced than in HF and accompanied by major alterations of JPH2 arrangement. Our study indicates that targeting sarcolemmal association of JPH2 might ameliorate age-associated deficiencies of heart function.

scholarly journals 112 THE AGE DEPENDENCY OF MYOCARDIAL EXCITATION CONTRACTION COUPLING

1985 ◽  
Vol 19 (4) ◽  
pp. 129A-129A
Author(s):  
Thomas S Klitzner ◽  
William F Friedman
Keyword(s):  
Age Dependency ◽  
Excitation Contraction Coupling ◽  
Contraction Coupling
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