scholarly journals Control of Ca Release Synchrony by Action Potential Configuration in Murine Cardiomyocytes

2010 ◽  
Vol 98 (3) ◽  
pp. 296a
Author(s):  
Johan Hake ◽  
Guro F. Jølle ◽  
Halvor K. Mørk ◽  
Ivar Sjaastad ◽  
Ole M. Sejersted ◽  
...  
Keyword(s):  
Action Potential ◽  
Action Potential Configuration

Inhibition of rest potentiation in canine ventricular muscle by BAY K 8644: comparison with caffeine

1989 ◽  
Vol 257 (2) ◽  
pp. H399-H406
Author(s):  
L. V. Hryshko ◽  
R. Bouchard ◽  
T. Chau ◽  
D. Bose
Keyword(s):  
Action Potential ◽  
Action Potential Duration ◽  
Calcium Uptake ◽  
Calcium Influx ◽  
Bay K 8644 ◽  
Contractile Apparatus ◽  
Peak Tension ◽  
Time To Peak ◽  
Configuration Changes ◽  
Action Potential Configuration

Rest potentiation, believed to be due to increased utilization of sarcoplasmic reticular calcium, was converted to rest depression by BAY K 8644 (1 microM). Plateau height and duration of the postrest beat were enhanced by BAY K 8644, suggesting an enhancement of extracellular calcium entry. Caffeine (3 mM) also produced depression at all rest intervals, although to a lesser extent than BAY K 8644. Compared with BAY K 8644, treatment with caffeine resulted in an elevation of plateau amplitude and a shortening of action potential duration. Action potential configuration changes induced by rest were unaltered by caffeine despite reduction in rest potentiation. Caffeine-induced rest depression was associated with an increase in the time to peak tension. This was not observed with BAY K 8644. Treatment with both caffeine (3 mM) and BAY K 8644 (1 microM) greatly prolonged time to peak tension. Action potential duration and plateau height were either maintained or increased. Less rest depression was observed with the combination than with either agent alone. These results suggest that 1) BAY K 8644 and caffeine inhibit rest potentiation by different mechanisms, and 2) caffeine-induced inhibition of calcium uptake by the sarcoplasmic reticulum may enhance the effect of BAY K 8644-induced increase in calcium influx on the contractile apparatus.

Acetate-induced depression of electrical and contractile activity in normoxic and hypoxic guinea pig papillary muscle

1989 ◽  
Vol 67 (7) ◽  
pp. 734-739
Author(s):  
Hideharu Hayashi ◽  
Hajime Terada ◽  
Alexander Kholopov ◽  
Terence F. McDonald
Keyword(s):  
Guinea Pig ◽  
Action Potential ◽  
Action Potential Duration ◽  
Contractile Activity ◽  
High Energy ◽  
Factors Affecting ◽  
Resting Tension ◽  
Tension Increase ◽  
Action Potential Shortening ◽  
Action Potential Configuration

The action potential configuration, developed tension, and resting tension were monitored in normoxic and hypoxic guinea pig papillary muscles superfused with solutions containing no substrate, glucose, or acetate (1–10 mM). In normoxic muscle, acetate provoked a concentration-dependent transient depression of the action potential duration and force of contraction, depression was maximal after 10–30 min, and recovery was complete after 90–120 min. In hypoxic muscle, acetate accelerated functional rundown (action potential shortening, decline of developed tension, increase in resting tension). Because rundown in hypoxic muscle was sensitive to factors affecting glycolysis (moderated by external glucose; accentuated by 2-deoxyglucose), the accentuated rundown with acetate may be accounted for by a partial block of glycolysis. However, block of glycolysis cannot explain the acetate-induced transient depression in normoxic muscle, since the depression was enhanced in normoxic muscle with 2-deoxyglucose-blocked glycolysis. We suggest that the transient depression is due to a transient depression of high energy nucleotides with consequent effects on ionic currents.Key words: acetate, action potential duration, 2-deoxyglucose, hypoxia, ATP.

Rate-dependent changes in cell shortening, intracellular Ca(2+) levels and membrane potential in single, isolated rainbow trout (Oncorhynchus mykiss) ventricular myocytes

2000 ◽  
Vol 203 (3) ◽  
pp. 493-504 ◽  
Author(s):  
C.L. Harwood ◽  
F.C. Howarth ◽  
J.D. Altringham ◽  
E. White
Keyword(s):  
Membrane Potential ◽  
Sarcoplasmic Reticulum ◽  
Action Potential ◽  
Ventricular Myocytes ◽  
Stimulation Frequency ◽  
Cell Shortening ◽  
Rainbow Trout Oncorhynchus Mykiss ◽  
Rate Dependent ◽  
Intracellular Ca ◽  
Action Potential Configuration

The effects of increasing stimulation frequency (from 0.2 to 1.4 Hz) on the contractility, intracellular Ca(2+) concentration ([Ca(2+)](i)) and membrane potential of single ventricular myocytes isolated from the heart of rainbow trout (Oncorhynchus mykiss) were measured. Cell shortening, expressed as a percentage of resting cell length, was our index of contractility. The fluorescent Ca(2+) indicator Fura-2 was used to monitor changes in [Ca(2+)](i). Action potentials and L-type Ca(2+) currents (I(Ca)) were recorded using the whole-cell patch-clamp technique. Experiments were performed at 15 degrees C. Increasing the stimulation frequency caused a significant increase in diastolic [Ca(2+)](i) and a significant decrease in diastolic cell length and membrane potential. During systole, there was a significant fall in the amplitude of the [Ca(2+)](i) transient, cell shortening and action potential with a decrease in the duration of the action potential at both 20 % and 90 % repolarisation. Caffeine was used to assess the Ca(2+) content of the sarcoplasmic reticulum. We observed that sarcoplasmic reticulum Ca(2+) load was greater at 1.0 Hz than at 0.6 Hz, despite a smaller electrically evoked [Ca(2+)](i) transient. The amplitude of I(Ca) was found to decrease with increased stimulation frequency. At 0.6 Hz, electrically evoked [Ca(2+)](i) transients in the presence of 10 mmol l(−)(1) caffeine or 10 micromol l(−)(1) ryanodine and 2 micromol l(−)(1) thapsigargin were reduced by approximately 15 %. We have described the changes in contractility, [Ca(2+)](i) and action potential configuration in a fish cardiac muscle system. Under the conditions tested (0.6 Hz, 15 degrees C), we conclude that the sarcoplasmic reticulum contributes at least 15 % of the Ca(2+) associated with the [Ca(2+)](i) transient. The rate-dependent decrease in contraction amplitude appears to be associated with the fall in the amplitude of the [Ca(2+)](i) transient. This, in turn, may be influenced by changes in the action potential configuration via mechanisms such as altered Ca(2+) efflux and Ca(2+) influx. In support of our conclusions, we present evidence that there is a rate-dependent decrease in Ca(2+) influx via I(Ca) but that the Ca(2+) load of the sarcoplasmic reticulum is not reduced at increased contraction frequencies.

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