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Effects of external calcium on potassium contractures in tonic muscle fibers of the frog (Rana pipiens).
Author(s) -
Huerta M,
Muñiz J,
Stefani E
Publication year - 1986
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1113/jphysiol.1986.sp016150
Subject(s) - tonic (physiology) , muscle contracture , chemistry , contracture , nifedipine , egta , potassium , biophysics , calcium , tension (geology) , medicine , endocrinology , anatomy , materials science , ultimate tensile strength , surgery , biology , organic chemistry , metallurgy
K+ contractures of tonic bundles from cruralis muscle of the frog were studied with different K+ concentrations (10‐120 mM). K+ contractures had an initial transient phase followed by a sustained tension. The amplitude of the sustained tension diminished with high K+ concentration (80‐120 mM). However, in all cases, tension was maintained for several minutes. External Ca2+ reduction practically abolished the sustained phase of the K+ contractures. The initial phase was also reduced and tension spontaneously relaxed. The curve relating the peak tension with log [K+]o, showed that the threshold was not affected but the peak tension was reduced to about 70% in low‐Ca2+ saline (0 Ca2+ + 3 mM‐Mg2+) and 50% in Ca2+‐free saline (1 mM‐EGTA + 3 mM‐Mg2+). The dependence of the sustained tension on external Ca2+ was further confirmed by Ca2+ withdrawal and re‐establishment and/or by Ni2+ substitution for Ca2+ before or during K+ contractures. These results indicate that external Ca2+ had to be continuously present to maintain the tension during K+ contractures and that Ni2+ was not able to restore the normal temporal course of K+ contracture. The sustained phase was diminished by blocking agents of Ca2+ channels, such as nifedipine (1 microM) and diltiazem (1‐10 microM). The present results can be explained by a direct control of the Ca2+ currents on K+ contracture or by specific interactions between external Ca2+ and Ca2+‐binding sites in the membrane.