Premium
Calcium‐induced release of strontium ions from the sarcoplasmic reticulum of rat cardiac ventricular myocytes
Author(s) -
Spencer C. Ian,
Berlin Joshua R.
Publication year - 1997
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 - 10.1111/j.1469-7793.1997.565bd.x
Subject(s) - endoplasmic reticulum , biophysics , ryanodine receptor , calcium , chemistry , caffeine , myocyte , divalent , voltage clamp , intracellular , strontium , voltage dependent calcium channel , membrane potential , medicine , endocrinology , biochemistry , biology , organic chemistry
1 The effects of strontium ions, Sr 2+ , on Ca 2+ ‐dependent feedback mechanisms during excitation‐contraction coupling were examined in voltage‐clamped rat ventricular myocytes in which intracellular [Ca 2+ ] and [Sr 2+ ] were monitored with the fluorescent indicator, indo‐1. 2 Voltage clamp depolarizations and caffeine applications during superfusion in Ca 2+ ‐free, Sr 2+ ‐containing solutions were employed to exchange intracellular Ca 2+ with Sr 2+ . Myocytes were loaded with Sr 2+ by applying voltage clamp depolarizations during superfusion in Na + ‐free, Sr 2+ ‐containing solutions. 3 Caffeine applications produced large fluorescence transients in Sr 2+ ‐loaded cells. Thus, Sr 2+ could be sequestered and released from the sarcoplasmic reticulum. 4 Ca 2+ influx, but not Sr 2+ influx, via sarcolemmal Ca 2+ channels evoked ryanodine‐sensitive fluorescence transients in Sr 2+ ‐loaded cells. These results demonstrated that Ca 2+ influx‐induced Sr 2+ release (CISR) from the sarcoplasmic reticulum occurred in these experiments, even though Sr 2+ influx‐induced Sr 2+ release was not observed. 5 The amplitude of the Ca 2+ influx‐induced fluorescence transient was 17 ± 1% of the caffeine‐induced transient ( n = 5 cells), an indication that fractional utilization of Sr 2+ sequestered in the sarcoplasmic reticulum during CISR was low. 6 With increased Sr 2+ loading, the amplitude of Ca 2+ influx‐ and caffeine‐induced fluorescence transients increased, but fractional utilization of sarcoplasmic reticulum divalent cation stores was independent of the degree of Sr 2+ loading. These data suggest that Ca 2+ influx directly activated the release of divalent cations from the sarcoplasmic reticulum, but mechanisms promoting positive feedback of Sr 2+ release were minimal during CISR. 7 By comparison, in Ca 2+ ‐loaded myocytes, Ca 2+ influx‐induced Ca 2+ release (CICR) utilized a greater fraction of caffeine‐releasable stores than CISR. Fractional utilization of Ca 2+ stores during CICR increased with the degree of Ca 2+ loading. 8 Taken together, these results suggest that Ca 2+ ‐dependent feedback mechanisms play a major role in determining the extent of sarcoplasmic reticulum Ca 2+ release during cardiac excitation‐contraction coupling under a wide range of conditions.