Paradox response of frog muscle membrane to changes in external potassium

1989 ◽  
Vol 414 (2) ◽  
pp. 157-161 ◽  
Author(s):  
P. P. N�n�si ◽  
M. Dank�
1978 ◽  
Vol 234 (3) ◽  
pp. C110-C114 ◽  
Author(s):  
R. J. Connett

The pH difference across the cell membrane of frog sartorius muscle cells was measured with the distribution of 5,5-dimethyl-2,4-oxazolidine-dione (DMO) as the marker. Depolarization of the muscles to values at or below the contraction threshold caused by elevating external potassium up to approximately 20 mM resulted in an internal alkalinization. The change was smaller with superthreshold depolarization (20--30 mM [K+]). The alkalinization was blocked by agents that block calcium release from the sarcoplasmic reticulum (procaine and dantrolene sodium). Other agents that cause calcium release (caffeine, theophylline, and quinine) were found to give alkalinization when tested at concentrations just below the contracture threshold. Increased acidification of the extracellular medium was associated with the internal alkalinization. The data were interpreted as indicating the presence of a calcium-stimulated H+ and/or OH- ion transport system in the muscle membrane.


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.


1960 ◽  
Vol 198 (1) ◽  
pp. 67-77 ◽  
Author(s):  
L. B. Smillie ◽  
J. F. Manery

In Ringer's solution containing 10 mEq K/l., frog muscles consumed oxygen at 20°C at rates ranging from 88 (summer frogs) to 128 (winter frogs) cu mm/gm/hr. These rates, which were three to four times higher than those at 2 and 6 mEq K/l., continued to rise for at least 6 hours, although the muscles had previously been soaked at 5°C in the type of Ringer's in which they respired. Addition of lactate increased the respiratory rate at all K concentrations studied. When insulin was present a marked additional stimulation was observed at 2 and 6 mEq K/l., which was changed to an inhibition at 10 mEq/l. Potassium analyses of all of the environmental fluids and of the muscles (144 of each) demonstrated a slight K loss from control muscles which was reduced or abolished by lactate. Insulin, however, either with or without added lactate, abolished the K loss and induced an appreciable K uptake. This K gain occurred regardless of the effect of insulin on the respiratory rate. Denaturation of the insulin abolished all of its effect. Seasonal differences were noted.


1960 ◽  
Vol 198 (6) ◽  
pp. 1360-1360
Author(s):  
L. B. Smillie ◽  
J. F. Manery

L. B. Smillie and J. F. Manery, "Effect of external potassium concentrations, insulin and lactate on frog muscle potassium and respiratory rate." Page 69: Table 1, Section 3, Insulin effect in the presence of lactate (May, June and July), column 3 (Exptl.) should read RIL for all solutions. Page 70: 1st column, 4th paragraph, 2nd sentence should read: A marked depression of the oxygen consumption. ... Page 71: 1st column, 3rd paragraph, 14th line should read: ... Ringer-lactate at the 5th and 6th hours being 136.9 and that in Ringer-insulin-lactate being 81.8 cu mm/gm/hr. Page 72: 1st column, 1st paragraph, 7th line should read: ... lactate when the metabolic changes invoked by high potassium were in operation. Page 73: 1st column, 2nd paragraph, 15th line should read: ... muscle and fluid analyses are presented in column 7. Page 73: 2nd column, 3rd paragraph, 6th line should read: That the depression of the potassium movement is specifically related to insulin and is unrelated to lactate is again implied. ... Page 74: 1st column, 1st paragraph, 8th line should read: ... the amounts of potassium taken from the medium. ... Page 76: 2nd column, 3rd paragraph, 9th line should read: ... that phosphocreatine began to be hydrolyzed. ... Page 77: Reference 1 should read: Manery, J. F., L. B. Smillie and K. E. Toye. J. Cell & Comp. Physiol. 44:336, 1954.


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.


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