Intramembrane Charge Frog Skeletal Muscle in Hypertonic Solutions Movements in Strongly

Intramembrane charge movements were studied in intact, voltageclamped frog (Rana temporaria) skeletal muscle fibers in external solutions made increasingly hypertonic by addition of sucrose. The marked dependence of membrane capacitance on test potential persisted with increases in extracellnlar sucrose concentration between 350 and 500 mM. Charge movements continued to show distinguishable early monotonic (qa) decays and the strongly voltage-dependent delayed (qv) charging phases reported on earlier occasions. In contrast, a further increase to 600 mM sucrose abolished the most steeply voltage-sensitive part of the membrane capacitance. It left a more gradual variation with potential that closely resembled the function that resulted when qv charge was abolished by tetracaine in the presence of 500 mM sucrose. Charging transients were now simple monotonic (qa) decays and lacked delayed (q~) transients. Furthermore, tetracaine (2 mM) altered neither the kinetic nor the steady-state features of the charge left in 600 mM sucrose. However, Ca 2÷ current activation in the same fibers persisted through such tonicity increases under identical conditions of temperature, external solution, and holding voltage. Tonicity changes thus accomplish an independent separation of qv and qa charge as defined hitherto through their tetracaine sensitivity. Their effects on q, charge correlate with earlier observations of osmotic conditions on A[Ca 2*] signals (1987. J. Physiol. (Lond.) 383:615-627.) and the parallel effects of other agents on excitation--contraction coupling and q, charge. In contrast, they suggest that Ca 2+ current activation does not require q, charge transfer whether by itself or as part of the excitation-contraction coupling process. I N T R O D U C T I O N An increasing amount o f evidence has implicated receptors for 1,4 dihydropyridine calcium channel antagonists in voltage-sensing processes in skeletal muscle. Nifedipine partially blocks both in t ramembrane charge and intracellular Ca 2+ signals elicited by depolarizing voltage clamp steps, particularly after small shifts in holding potential (Rios and Brum, 1987). Charge movements in turn have been resolved into several components on the basis of their voltage and pharmacological sensitivities Address reprint requests to Dr. C. Huang, Physiological Laboratory, Downing Street, Cambridge CB2 3EG, UK. J. G~N. Pro'SlOE. © The Rockefeller University Press • 0022-1295/92/04/0531/14 $2.00 Vo|ume 99 April 1992 531-544 531 on Jne 0, 2017 D ow nladed fom Published April 1, 1992