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Biophys J. 2008 Aug;95(3):1412-27. doi: 10.1529/biophysj.108.130385. Epub 2008 Apr 4.

Ca2+-mobility in the sarcoplasmic reticulum of ventricular myocytes is low.

Author information

1
Burdon Sanderson Cardiac Science Centre, Department of Physiology, Anatomy, and Genetics, Oxford University, Oxford OX1 3PT, United Kingdom.

Abstract

The sarcoplasmic reticulum (SR) in ventricular myocytes contains releasable Ca(2+) for activating cellular contraction. Recent measurements of intra-SR (luminal) Ca(2+) suggest a high diffusive Ca(2+)-mobility constant (D(CaSR)). This could help spatially to unify SR Ca(2+)-content ([Ca(2+)](SRT)) and standardize Ca(2+)-release throughout the cell. But measurements of localized depletions of luminal Ca(2+) (Ca(2+)-blinks), associated with local Ca(2+)-release (Ca(2+)-sparks), suggest D(CaSR) may actually be low. Here we describe a novel method for measuring D(CaSR). Using a cytoplasmic Ca(2+)-fluorophore, we estimate regional [Ca(2+)](SRT) from localized, caffeine-induced SR Ca(2+)-release. Caffeine microperfusion of one end of a guinea pig or rat myocyte diffusively empties the whole SR at a rate indicating D(CaSR) is 8-9 microm(2)/s, up to tenfold lower than previous estimates. Ignoring background SR Ca(2+)-leakage in our measurement protocol produces an artifactually high D(CaSR) (>40 microm(2)/s), which may also explain the previous high values. Diffusion-reaction modeling suggests that a low D(CaSR) would be sufficient to support local SR Ca(2+)-signaling within sarcomeres during excitation-contraction coupling. Low D(CaSR) also implies that [Ca(2+)](SRT) may readily become spatially nonuniform, particularly under pathological conditions of spatially nonuniform Ca(2+)-release. Local control of luminal Ca(2+), imposed by low D(CaSR), may complement the well-established local control of SR Ca(2+)-release by Ca(2+)-channel/ryanodine receptor couplons.

PMID:
18390622
PMCID:
PMC2479570
DOI:
10.1529/biophysj.108.130385
[Indexed for MEDLINE]
Free PMC Article

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