AJP - Cell Physiology, Vol 258, Issue 6 C1165-C1168, Copyright © 1990 by American Physiological Society
Local activation of contraction in isolated rat ventricular myocytes
S. C. O'Neill, J. G. Mill and D. A. Eisner
Department of Physiology, University College London, United Kingdom.
The aim of this paper was to examine whether contraction (which is thought
to result from Ca-induced release of Ca2+ from the sarcoplasmic reticulum)
can propagate along a cardiac cell. The experiments were performed on
isolated rat ventricular cardiac myocytes. Two techniques were used to
initiate contraction in a localized region of the cell. 1) The cells were
loaded with the "caged" Ca-containing compound nitr-5. A region of the cell
was illuminated with ultraviolet light to increase intracellular Ca2+
concentration ([Ca2+]i) in that area. 2) The cells were superfused with a
low (0.1 mM) Ca solution to abolish contraction. Ca was applied to a region
of the cell by iontophoresis, and the cell was then electrically
stimulated. In both cases a local contraction was produced that did not
spread to the rest of the cell. Like the normal twitch, the local
contraction was abolished by ryanodine, showing that it is produced by Ca
release from the sarcoplasmic reticulum. In the final series of
experiments, the cell was stimulated to contract in a control (1 mM Ca2+)
solution. Cd2+ was then iontophoresed to a region of the cell. Only the
region of the cell exposed to Cd stopped contracting. In conclusion, the
above results show that the systolic rise of [Ca2+]i cannot propagate
through a cell. This lack of propagation is suggested to be important in
stopping a rise of [Ca2+]i in one cell spreading to the rest of the heart.
