Sodium movements in denervated muscle and the effects of antimycin A

Abstract

SUMMARY1. Fibre sodium in rat diaphragm exchanged at a faster rate in muscles which had been denervated 8 days previously. The half-time was 3-7 min for outward movement in denervated muscles and 5*1 min in controls.2. The inward movement of sodium was also faster in denervated muscle as compared with controls, and the calculated permeability to sodium was approximately doubled.3. In the presence of antimycin A (1-8 x 10-5 M), the outward movement of sodium in denervated diaphragm was slowed and the fibres gained sodium and lost potassium.4. Antimycin markedly reduced the twitch produced by stimulation of denervated diaphragm, and also the response to acetylcholine. Similar effects were found in denervated tibialis anterior of the cat.

Cellular ions in intact and denervated muscles of the rat

“…Intracellular measured sodium and chloride activities also increase. Analysis of our data supports the hypothesis (Creese et al, 1968;Robbins, 1977;Wareham, 1978;Shabunova & Vyskocil, 1982) that relative to membrane permeability to potassium, membrane permeability to sodium is increased by denervation, …”

“…However, they favor an alternate hypothesis--that the denervation results in an increased membrane permeability to sodium relative to potassium as proposed by others (Creese et al, 1968;Robbins, 1977;Wareham, 1978;Shabunova & Vyskocil, 1982). Not only did the denervated fibers contain more sodium (together with chloride and water to maintain electroneutrality and isosmolality, respectively (Tables 1 and 3), whether this change was determined by activity measurements or by chemical analysis (Table 6), but they gained sodium and lost potassium over 40 rain when metabolism was suppressed by chilling and anoxia (Table 5), whereas the innervated muscles maintained their composition under these conditions.…”

“…However, chemical analysis of innervated and denervated rat skeletal muscle has not revealed any significant decrease in estimated cellular potassium concentration (Fenn, 1937;Lullmann, 1958;Creese et al, 1968;Robbins, 1977). If cellular potassium is unaltered, a decreased activity would require that potassium be in some way sequestered or 'bound' as a consequence of denervation (Ware et al, 1954).…”

“…Whatever the underlying mechanism, such a decrease must reflect some alteration in ion movements across the cellular membranes. Possibilities suggested include a change in passive membrane permeability (Creese, E1-Shafie & Vebova, 1968;Robbins, 1977;Wareham, 1978;Shabunova & Vyskocil, 1982), a decrease in the contribution of a rheogenic pump to the resting potential (Locke & Soloman, 1967;Albuquerque et al, 1971;McArdle & Albuquerque, 1975;Bray et al, 1976;Sellin & McArdle, 1977) or a decreased contribution to potential from potassium diffusion (Albuquerque & McIsaac, 1970).…”

Decamethonium in depolarized muscle and the effects of tubocurarine

“…From the results of Creese, El-Shafie & Vrbova (1968) and the formulas used by them, the permeability of decamethonium may be compared with that of sodium and potassiurm if these ions can be treated as though they moved independently down…”