AJP - Heart Calcium Transients and Cell-Sarcomere
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Am J Physiol Heart Circ Physiol 271: H1814-H1822, 1996;
0363-6135/96 $5.00
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AJP - Heart and Circulatory Physiology, Vol 271, Issue 5 1814-H1822, Copyright © 1996 by American Physiological Society

ARTICLES

Reloading of Ca(2+)-depleted sarcoplasmic reticulum during rest in guinea pig ventricular myocytes

C. M. Terracciano and K. T. MacLeod
Imperial College of Science, Technology and Medicine, National Heart and Lung Institute, London, United Kingdom.

The effects of rest on a Ca(2+)-depleted sarcoplasmic reticulum (SR) in guinea pig ventricular myocytes were investigated. Cell shortening was measured using a video edge-detection system, and cytoplasmic Ca2+ was monitored using the fluorescent indicator indo-1. Rapid cooling and rewarming in the presence of 10 mM caffeine were used to deplete the SR of Ca2+. The resting cell was then superfused for variable time intervals with a normal Tyrode solution containing 2 mM Ca2+. Another rapid cooling in caffeine was performed to assess the SR Ca2+ load at the end of rest. Rapid cooling after 1- and 2-min rest elicited an increase of indo-1 fluorescence of 51.9 +/- 7.7 (n = 17) and 72.7 +/- 6.7% of control (n = 9), respectively. This increase was not detectable when Ca2+ was absent from the superfusing solution. In contrast, the increase was larger when external Ca2+ was elevated to 4 mM. Nickel (5 mM) and nifedipine (20 microM) added to the superfusing solution during the rest interval did not alter the increase in indo-1 fluorescence. We conclude that Ca2+ is reaccumulated by a depleted SR during rest. Although this Ca2+ seems to originate from the extracellular space, its route from there to the SR is unclear.


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