Adenosine inhibits depolarization-induced Ca(2 ) release in mammalian skeletal muscle.

Abstract

In normal skeletal muscle, prolonged stimulation results in some cellular adenosine triphosphate (ATP) being converted to adenosine monophosphate (AMP) and then deaminated to inosine monophosphate (IMP). Here, we investigate whether the build-up of IMP contributes to muscle fatigue and also determine what happens if AMP is instead hydrolyzed to adenosine. Rat skeletal muscle fibers were mechanically skinned, allowing rapid manipulation of the cytoplasmic conditions, while still retaining the normal excitation-contraction coupling mechanism. Inosine monophosphate (3 mM) had no noticeable effect on either depolarization-induced or caffeine-induced Ca(2+) release from the sarcoplasmic reticulum..