Affiliation:
1. From the Unit of Cardiac Physiology, University of Manchester, Manchester, UK.
Abstract
Abstract
—The aim of this study was to investigate how sarcoplasmic reticulum (SR) Ca
2+
content and systolic Ca
2+
are controlled when Ca
2+
entry into the cell is varied. Experiments were performed on voltage-clamped rat and ferret ventricular myocytes loaded with fluo-3 to measure intracellular Ca
2+
concentration ([Ca
2+
]
i
). Increasing external Ca
2+
concentration ([Ca
2+
]
o
) from 1 to 2 mmol/L increased the amplitude of the systolic Ca
2+
transient with no effect on SR Ca
2+
content. This constancy of SR content is shown to result because the larger Ca
2+
transient activates a larger Ca
2+
efflux from the cell that balances the increased influx. Decreasing [Ca
2+
]
o
to 0.2 mmol/L decreased systolic Ca
2+
but produced a small increase of SR Ca
2+
content. This increase of SR Ca
2+
content is due to a decreased release of Ca
2+
from the SR resulting in decreased loss of Ca
2+
from the cell. An increase of [Ca
2+
]
o
has two effects: (1) increasing the fraction of SR Ca
2+
content, which is released on depolarization and (2) increasing Ca
2+
entry into the cell. The results of this study show that the combination of these effects results in rapid changes in the amplitude of the systolic Ca
2+
transient. In support of this, the changes of amplitude of the transient occur more quickly following changes of [Ca
2+
]
o
than following refilling of the SR after depletion with caffeine. We conclude that the coordinated control of increased Ca
2+
entry and greater fractional release of Ca
2+
is an important factor in regulating excitation-contraction coupling.
Publisher
Ovid Technologies (Wolters Kluwer Health)
Subject
Cardiology and Cardiovascular Medicine,Physiology
Cited by
89 articles.
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