Aspects of pHi Regulation in Frog Skeletal Muscle

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Intracellular pH (pHi) in cells is higher than it would be if H ions were in electrochemical equilibrium. At steady state, this high pHi is maintained by acidifying influences—such as H influx, metabolic acid production, and HCO3 efflux—suggesting the presence of active transport systems that remove acid equivalents from the cell. This chapter describes the results of studies on pHi regulation in frog skeletal muscle and the changes affecting the steady state pHi. It also describes the properties of the membrane transport systems responsible for pHi regulation and some factors that can modify this regulation. In addition, a comparison between pHi regulation in frog muscle with that in other cells is presented. The membrane transport systems responsible for pHi recovery from acid load in frog muscle fibers are (1) Na–H exchange that can be inhibited by amiloride or by removal of Na from the external medium, and (2) a system that requires HC03, Cl, and Na, can be inhibited by 4-acetamide-4′-isothiocyanatostilbene-2,2′-disulfonic acid (SITS). The Na–H exchanger seems to be equally active in normally polarized and depolarized fibers, whether they are acidified by CO2 or by an NH4Cl prepulse. The SITS-sensitive component manifests itself when the fibers are acidified and depolarized. The resulting elevation of intracellular Cl may be necessary for the appearance of this component of recovery. When normally polarized cells are acidified with CO2, an acidifying HCO3 efflux masks the pHi recovery. The Na–H exchanger in frog muscle is comparable to that in a variety of other vertebrate cells, while the SITS-sensitive component may be more similar to that found in invertebrate nerve and muscle cells.



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