Affiliation:
1. Department of Physiology, University College London, UnitedKingdom.
Abstract
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.
Publisher
American Physiological Society
Cited by
50 articles.
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