Effect of Pharmacological Agents on Calcium Stores in Amphibian Fast and Slow Muscle Fibers

Abstract

Amphibian fast and slow muscles muscle fibers differ in regard to structure, innervation, and contractile response. These differences can be utilized to study drug effects on cellular Ca2+ metabolism. The amphibian slow muscle fiber contains multiple end plates, is innervated by small nerve fibers, and gives a graded tonic response to repetitive neural stimulation. Tension is regulated by graded levels of depolarization of the surface membrane (Kuffler and Williams, 1953a, 1953b). Identical contractures produced by K+ depolarization or acetylcholine are associated with a sustained increase in Ca2+ influx, a transient increase in Ca2+ efflux and a net gain of Ca2+ which amounts to 0.24 µmol/g for the KC1 contracture and 0.27 µmol/g for the acetylcholine contracture (Bianchi, 1968a). During relaxation the Ca2+ becomes sequestered within the sarcoplasmic reticulum of the slow muscle fibers. The sarcoplasmic reticulum of the amphibian slow muscle fiber lacks the triad structure of the amphibian fast muscle fiber, but does contain invaginations of the cell membrane which extend into the cell interior and run in a longitudinal fashion parallel to the fiber axis (Page, 1965). The primary function of the sarcoplasmic reticulum present in the amphibian slow muscle fiber is to allow for rapid relaxation following the shutting off of Ca2+ influx during repolarization of the surface membrane. In the relaxed state Ca2+ efflux must exceed influx in order to restore the fiber Ca2+ content to steady state conditions.