ArticleThe Journal of physiology2003
pH-dependent and -independent effects inhibit Ca(2+)-induced Ca2+ release during metabolic blockade in rat ventricular myocytes.
Article in The Journal of physiology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Regional acidosis locally inhibits but remotely stimulates Ca2+ waves in ventricular myocytes.Cardiovascular research · 2017Article
- Metabolic inhibition reduces cardiac L-type Ca2+ channel current due to acidification caused by ATP hydrolysis.PloS one · 2017Article
- Acetate transiently inhibits myocardial contraction by increasing mitochondrial calcium uptake.BMC physiology · 2014Article
- Effect of metabolic inhibition on couplon behavior in rabbit ventricular myocytes.Biophysical journal · 2008Article
- Interplay between SERCA and sarcolemmal Ca2+ efflux pathways controls spontaneous release of Ca2+ from the sarcoplasmic reticulum in rat ventricular myocytes.The Journal of physiology · 2004Article
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2 authors.
Funding
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Abstract
We have investigated the role of changes of intracellular pH (pHi) in the effects of metabolic blockade (cyanide plus 2-deoxyglucose) on Ca2+ release from the sarcoplasmic reticulum (SR) in rat ventricular myocytes. pHi and cell length were measured simultaneously. Metabolic blockade decreased the frequency of Ca2+ waves, an effect previously shown to be due to inhibition of Ca2+ release from the SR. This was accompanied by an intracellular acidification. Intracellular acidification was produced in the absence of metabolic inhibition by application of sodium butyrate. A maintained intracellular acidosis produced a decrease of wave frequency. A hysteresis between pHi and wave frequency was observed such that during the onset of the acidification the wave frequency decreased more than in the steady state. Comparison of the steady state relationship between pHi and wave frequency showed that the decrease of wave frequency produced by metabolic blockade was greater than could be accounted for simply by the accompanying decrease of pHi. In other experiments the buffering power of the solution was increased. Under these conditions, metabolic blockade produced no change of pHi but the decrease of wave frequency persisted. We conclude that, although intracellular acidification occurs during metabolic blockade, it is not responsible for most of the inhibition of Ca2+ release from the SR.
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