Re-loading of ca2+ depleted sarcoplasmic reticulum during rest in
guinea-pig ventricular myocytes.
Terracciano, Cesare M. N., and Kenneth T. Macleod.
Imperial College of Science, Technology and Medicine, National
Heart & Lung Institute, Cardiac Medicine, Dovehouse Street, London
SW3 6LY, U.K.
APStracts 3:0213H, 1996.
The effects of rest on a Ca2+ 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 minute and 2 minutes
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 in the superfusing
solution. In contrast the increase was larger when external Ca2+ was
elevated to 4 mM. 5 mM nickel and 20 [mu]M nifedipine added to the
superfusing solution during the rest interval did not alter the
increase in indo-1 fluorescence. We conclude that Ca2+ is re
-accumulated 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.
Received 9 February 1996; accepted in final form 7 May 1996.
APS Manuscript Number H127-6.
Article publication pending Am. J. Physiol. (Heart Circ. Physiology).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 5 June 96