Parvalbumin is overexpressed in the late phase of pharmacological preconditioning in skeletal muscle.

Pharmacological preconditioning (PPC) with mitochondrial ATP-sensitive K+ channel openers such as diazoxide, provides protection against ischemia in cardiac muscle, skeletal muscle, and other tissues. Effects on Ca2+ homeostasis during the late phase of PPC have been described in cardiomyocytes, but no information is available regarding intracellular Ca2+ changes in skeletal muscle fibers during late PPC. Intracellular Ca2+ signals were measured in single fibers of adult mouse skeletal muscle, with fluorescent probes, 48 h after the administration of diazoxide. Parvalbumin levels in the myofibers were quantitated by Western blot. Diazoxide induction of late PPC was confirmed by partial protection of muscles from peroxide-induced damage. Late PPC was associated with a significant decrease in the duration of Ca2+ signals during single twitches and tetanus with no changes in peak values. This effect was prevented by the reactive oxygen species (ROS) scavenger tiron. Late PPC was accompanied by a 30% increase in parvalbumin levels, and this effect was also blocked by tiron. Our data show, for the first time, a role of parvalbumin in late PPC in skeletal muscle. [ABSTRACT FROM AUTHOR]