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British Journal of Pharmacology logoLink to British Journal of Pharmacology
. 1977 Dec;61(4):627–638. doi: 10.1111/j.1476-5381.1977.tb07556.x

The role of extracellular calcium in the contractions produced by acetylcholine in chronically denervated muscle

Moira T Hall, MA Maleque, RM Wadsworth
PMCID: PMC1668078  PMID: 413600

Abstract

1 Acetylcholine-induced contractions of the isolated chronically denervated soleus muscle of the mouse consist of two phases, but both phases are equivalent to the contracture phase seen in vivo.

2 Low [Ca2+]0 (0.5-1.5 mM) augmented peak tension, as well as the rate of relaxation, of the first phase, but inhibited the second phase. Ethyleneglycol-bis-(β-aminoethyl ether)-N,N'-tetraacetic acid (EGTA) or La3+ (2 mM) also inhibited the second phase, but not the first.

3 It was concluded that the first phase requires Ca2+ release from the sarcoplasmic reticulum, and is terminated by inactivation of the contractile process. The second phase is caused by the entry of activator Ca2+ from the extracellular space.

4 Increasing [Ca2+]o to 5 or 10 mM after the addition of acetylcholine caused a contraction, starting after a delay of about 50 seconds. EGTA or La3+ added during the second phase of the acetylcholine contraction caused relaxation after a much shorter lag time.

5 It is concluded that most of the Ca2+ entering from the extracellular fluid is taken up by the sarcoplasmic reticulum.

6 The acetylcholine second phase was augmented in low (25 mM) [Na+]0. It is concluded that Na+ and Ca2+ compete for the acetylcholine controlled ionic channels.

7 Isolated chronically denervated diaphragm muscles were less sensitive to acetylcholine and the contraction usually consisted of a first phase only.

8 It is concluded that sequestration of Ca2+ entering from the extracellular fluid is more complete in the diaphragm.

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Selected References

These references are in PubMed. This may not be the complete list of references from this article.

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