Changes of SERCA activity have only modest effects on sarcoplasmic reticulum Ca 2+  content in rat ventricular myocytes | Zendy

Bode E. F. | Zendy; Briston S. J. | Zendy; Overend C. L. | Zendy; O’Neill S. C. | Zendy; Trafford A. W. | Zendy; Eisner D. A. | Zendy

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Changes of SERCA activity have only modest effects on sarcoplasmic reticulum Ca 2+ content in rat ventricular myocytes

Author(s) -

Bode E. F.,

Briston S. J.,

Overend C. L.,

O’Neill S. C.,

Trafford A. W.,

Eisner D. A.

Publication year - 2011

Publication title -

the journal of physiology

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 1.802

H-Index - 240

eISSN - 1469-7793

pISSN - 0022-3751

DOI - 10.1113/jphysiol.2011.211052

Subject(s) - serca , thapsigargin , endoplasmic reticulum , ryanodine receptor , chemistry , medicine , endocrinology , contractility , myocyte , biophysics , atpase , biology , biochemistry , enzyme

Non‐Technical Summary Cardiac contraction is caused by an increase of calcium (Ca 2+ ) concentration in the cells of the heart, the so‐called ‘systolic Ca 2+ transient’. The majority of this Ca 2+ is provided by the sarcoplasmic reticulum (SR), which acts as a Ca 2+ store within the cell itself. Before the heart can contract again the Ca 2+ store needs to be replenished and so Ca 2+ is pumped back into the SR by the sarco‐endoplasmic reticulum Ca 2+ ‐ATPase (SERCA). We show that a given fractional decrease of SERCA activity produces a much smaller decrease of SR Ca 2+ content. This means that changes of SERCA activity can produce large changes of systolic Ca 2+ without the need for energetically expensive alterations of SR Ca 2+ content.

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