Cellular Calcium Movements and Excitation-Contraction Coupling in Guinea Pig Atria
Burton, John Todd
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https://hdl.handle.net/2142/72406
Description
Title
Cellular Calcium Movements and Excitation-Contraction Coupling in Guinea Pig Atria
Author(s)
Burton, John Todd
Issue Date
1993
Doctoral Committee Chair(s)
Sleator, William,
Department of Study
Center for Biophysics and Computational Biology
Discipline
Biophysics
Degree Granting Institution
University of Illinois at Urbana-Champaign
Degree Name
Ph.D.
Degree Level
Dissertation
Keyword(s)
Biology, Cell
Biology, Animal Physiology
Biophysics, Medical
Abstract
Guinea pig left atria were suspended in a tissue bath of normal Krebs-Henseleit solution which was aerated with 95% O$\sb2$/5% CO$\sb2$ and maintained at 27$\sp\circ$C. The atria were attached to a force transducer and impaled with calcium sensitive micro-electrodes. The tissue was stimulated through 2 AgCl electrodes at 2 pulses per second (pps). When the tissue had reached a steady-state of contraction strength, rest intervals of 1 minute were introduced and the changes in the paracellular calcium levels were measured with the calcium sensitive micro-electrodes. The control condition produced an average increase during the interval in paracellular calcium concentration of 23.6 + 1.33 uM. Following treatment of the tissue with 8uM $3\sp\prime, 4\sp\prime$-di-chlorobenzamil (DCB), the average increase in paracellular calcium was 9.02 + 1.25 uM. DCB reduces the normal calcium efflux by 61.6 + 7.3%, n = 4, p $<$ 0.005. (Statistical analysis used paired one tail T-test.) 10 nM Ryanodine treated-tissue showed an increased efflux of calcium as measured by increased para-cellular calcium concentration of 9.8 + 1.9 uM over the control condition. 8uM DCB decreased the ryanodine treated tissues calcium efflux by 53.6 + 8.0%, n = 6, p $<$ 0.005, as measured by a decrease in the paracellular calcium concentration of 10.4 + 1.8 uM compared to the ryanodine treated condition. The cellular calcium efflux may be calculated from the measured changes in paracellular calcium concentration assuming an extracellular space of 47.8 ml/100 gm tissue. 8 uM DCB decreased the calcium efflux by 11.6 nmoles/sec per 100 gm tissue in non-ryanodine treated atria, and by 8.3 nmoles/sec per 100 gm of tissue in ryanodine treated atria. We conclude that DCB is an inhibitor of sodium-calcium exchange in guinea pig atria and that a measurable increase in paracellular calcium occurs during rest due to efflux of calcium from the cells via sodium-calcium exchange. In addition, we have shown that DCB decreases post-rest beat potentiation and this may indicate that sodium-calcium exchange plays a role in post-rest beat potentiation as well as the excitation-contraction coupling process.
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