scholarly journals The interaction of potassium with the activation of anomalous rectification in frog muscle membrane.

1981 ◽  
Vol 317 (1) ◽  
pp. 497-508 ◽  
Author(s):  
S Hestrin
1965 ◽  
Vol 48 (6) ◽  
pp. 1003-1010 ◽  
Author(s):  
D. C. Hellam ◽  
D. A. Goldstein ◽  
L. D. Peachey ◽  
W. H. Freygang

The late after-potential that follows trains of impulses in frog muscle fibers is virtually absent when most of the intracellular potassium is replaced by rubidium and the muscle is immersed in rubidium-containing Ringer's fluid. Its amplitude is also reduced in freshly dissected, potassium-containing muscle fibers that are immersed directly in Rb-Ringer's fluid. These findings are discussed in terms of the model for muscle membrane of Adrian and Freygang (1962 a, b) and in relation to the report of Adrian (1964) that Rb-containing muscle fibers do not exhibit the variations in potassium permeability as a function of membrane potential that are found in fibers with normal intracellular potassium concentration immersed in Ringer's fluid.


1962 ◽  
Vol 46 (1) ◽  
pp. 97-115 ◽  
Author(s):  
Shigehiro Nakajima ◽  
Shizuko Iwasaki ◽  
Kunihiko Obata

Delayed rectification was elicited in frog's skeletal muscles bathed in choline-Ringer's solution, in normal Ringer's solution with tetrodotoxin, in 40 mM Na2SO4 solution with tetrodotoxin, and even in 40 mM K2SO4 solution when the membrane had been previously hyperpolarized. However, after a sustained depolarization current-voltage relations in 40 mM K2SO4 and in 40 mM Na2SO4 solutions revealed a rectifier property in the anomalous direction. This indicates that the increase in potassium conductance which is brought about upon depolarization is a transient phenomenon and is inactivated by a maintained depolarization, and that this potassium inactivation process converts the delayed rectification into the anomalous rectification. In normal Ringer's solution with tetrodotoxin and in the 40 mM Na2SO4 solution with tetrodotoxin the apparent resistance was increased when the membrane was hyperpolarized beyond about -150 mv. This is thought to be due to a decrease of K conductance caused by a strong hyperpolarizing current. In the 40 mM Na2SO4 solution with tetrodotoxin a de- or hyperpolarizing current pulse induced a prolonged depolarizing response. During the early phase of this response the effective resistance was lower, and during the following phase greater than that in the resting fiber. An interpretation in terms of the ionic hypothesis was made of the nature of this response.


1969 ◽  
Vol 45 (9) ◽  
pp. 814-819 ◽  
Author(s):  
Kimihisa TAKEDA ◽  
Yutaka OOMURA

1983 ◽  
Vol 339 (1) ◽  
pp. 253-271 ◽  
Author(s):  
W Almers ◽  
P R Stanfield ◽  
W Stühmer

1972 ◽  
Vol 50 (5) ◽  
pp. 432-444 ◽  
Author(s):  
J. R. Riordan ◽  
J. F. Manery ◽  
E. E. Dryden ◽  
T. S. Still

Isolated frog muscles were exposed to concentrations of ethacrynic acid (2,3-dichloro-4-(2-methylene-butyryl)phenoxyaceticacid)ranging from 10−8 to 10−2 M. The diuretic (EA) at a concentration (10−3 M) which is sufficient to markedly inhibit net Na and K movements had no effect on three muscle surface enzymes (ATPase, adenylate kinase, 5′-AMP deaminase). The minimum concentration of EA required for inhibition of Na and K movement lies within the narrow range of 0.2 × 10−3 M to 10−3 M. The degree of inhibition increased with EA concentration up to 10−2 M. Concentrations of 0.2 × 10−3 M caused some contracture of the muscles as well. EA causes an increased K loss over that caused by ouabain alone both in the presence and absence of external Na. Na concentrations are not affected. Ouabain causes increased K loss over that caused by EA alone both in the presence and absence of external Na. Frog muscle has a component of K movement (about 35% of the total concentration) dependent upon external Na. This component is distinct from the ouabain-inhibited component and equal to the EA-inhibited component. The results are consistent with inhibition of the active transport of Na and K by EA as well as by ouabain and suggest that in the presence of Ca, EA also increases the passive permeability of the muscle membrane to K.


1962 ◽  
Vol 163 (1) ◽  
pp. 61-103 ◽  
Author(s):  
R. H. Adrian ◽  
W. H. Freygang

1961 ◽  
Vol 37 (8) ◽  
pp. 505-508 ◽  
Author(s):  
Shigehiro NAKAJIMA ◽  
Shizuko IWASAKI ◽  
Kunihiko OBATA

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