scholarly journals The intracellular pH of frog skeletal muscle: its regulation in hypertonic solutions.

1983 ◽  
Vol 345 (1) ◽  
pp. 189-204 ◽  
Author(s):  
R F Abercrombie ◽  
A Roos
1996 ◽  
Vol 271 (4) ◽  
pp. C1358-C1366 ◽  
Author(s):  
R. W. Putnam

Intracellular pH regulation was studied in semitendinosus muscle fibers from frog (Rana pipiens). Intracellular pH (pHi) was measured with recessed-tip glass microelectrodes and membrane potential with conventional microelectrodes. Fibers had their connections between the surface and transverse tubular membrane disrupted (detubulation) with the formamide shock technique. Fibers were approximately 80% detubulated as determined by the decrease in membrane capacitance and the loss of contractile capability. The initial rate of pHi recovery from acidification to approximately 6.8 (no CO2) was dependent on external buffering power, reaching a maximum of approximately 0.6 pH/h at 50 mM HEPES, indicating that the rate of pHi recovery in frog muscle is limited by the diffusion of buffer through an external "unstirred layer". In detubulated fibers, pHi recovery from acidification due to both the amiloride-sensitive Na+/H+ and the 4-acetamido-4'-isothiocyanostilbene-2,2'-disulfonic acid (SITS)-sensitive (Na+ + HCO3-)/Cl- exchangers was nearly identical to recovery in fully tubulated fibers. This is consistent with these two pH recovery transporters being localized to the surface, and not the transverse tubular, membrane domain in frog skeletal muscle fibers.


2001 ◽  
Vol 536 (2) ◽  
pp. 351-359 ◽  
Author(s):  
Sangeeta Chawla ◽  
Jeremy N. Skepper ◽  
Austin R. Hockaday ◽  
Christopher L.‐H. Huang

Author(s):  
Joachim R. Sommer ◽  
Nancy R. Wallace

After Howell (1) had shown that ruthenium red treatment of fixed frog skeletal muscle caused collapse of the intermediate cisternae of the sarcoplasmic reticulum (SR), forming a pentalaminate structure by obi iterating the SR lumen, we demonstrated that the phenomenon involves the entire SR including the nuclear envelope and that it also occurs after treatment with other cations, including calcium (2,3,4).From these observations we have formulated a hypothesis which states that intracellular calcium taken up by the SR at the end of contraction causes the M rete to collapse at a certain threshold concentration as the first step in a subsequent centrifugal zippering of the free SR toward the junctional SR (JSR). This would cause a) bulk transport of SR contents, such as calcium and granular material (4) into the JSR and, b) electrical isolation of the free SR from the JSR.


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