SUMMARY1. Extracellular pH (pH.) and intracellular pH (pHi) of superficial fibres of the rat soleus muscle were measured in vitro using pH-sensitive glass micro-electrodes. The origin of the pH gradient existing between the bulk--phaseofextracellular solution and the surface of muscle fibres was investigated.2. The pHo decreased almost linearly over a distance of 285 ,um from bulk solution to fibre surface. The magnitude of the bulk-surface pH gradient is greater in the mid region of the muscle than close to the tendon.3. Decreasing the superfusate velocity increased the magnitude of the pH gradient. Reducing the buffer capacity of the superfusing solution had the same effect.4. Inhibiting the aerobic metabolism or stimulating it acidified the fibre surface. Inhibiting glycolysis alone, or both aerobic metabolism and glycolysis, alkalinized the fibre surface.5. Inhibiting the membrane ionic exchange process involved in pHi regulation had no effect on surface pH.6. Changing the rate of aerobic or anaerobic metabolism quickly modified pHi in most cases.7. In conclusion the bulk-surface pH gradient seems to result mainly from diffusion of CO2 and lactic acid across an unstirred layer of fluid covering the surface of muscle fibres.
SUMMARY1. The membrane potential of isolated frog muscle fibres has been measured in absence and in presence of CO2, at constant external pH.2. At a normal external Cl concentration, CO2 (Pco2 = 97 mmHg; pH = 7.0) applied for 10 min caused a highly variable depolarization, the average potential change being 8 mV after 5 min. The effect was reversible.3. In Cl-free solutions, CO2 (P,02 = 97 mmHg; pH = 7.0) caused a biphasic depolarization of 20 mV after 5 min. The effect was fully reversible on CO2 removal.4. The same effect appeared at a lower partial pressure (PCO2 = 38 mmHg; pH 7 3) in the presence of tetrodotoxin (10-7 M).5. In order to investigate the cause of the CO2-induced depolarization, membrane potential and intracellular K activity (ak,) of surface muscle fibres were measured with voltage and ion-sensitive micro-electrodes. 6. At a normal external Cl concentration, CO2(P002 97 mmHg; pH = 7.0) decreased a' by 5 mm after 5 min.7. The same effect appeared at low external Cl concentration (11 mM). 8. At high partial pressure (P002 588 mmHg; pH = 6 8), CO2 reduced ak by 19 mM in 10 min.9. In long-term experiments performed over 4 h with a normal external Cl concentration, CO2 (PCO = 97 mmHg; pH 5-8 or 7) changed practically neither membrane potential, nor ak.10. It is concluded that increasing the PcO2 when keeping the external pH constant causes an early depolarization of muscle. This effect is particularly marked in the absence of chloride. It can be explained partly, in surface muscle fibres, by a decrease of the intracellular K activity.
1. The membrane potential of frog skeletal muscle was measured in various solutions, in the presence and in the absence of the CO2/HCO3- buffer. 2. The CO2/HCO3- buffer (PCO2 = 38-593 mm Hg; [HCO3-] = 5-25 mM/1) generally induced a reversible depolarization. 3. In the presence of C1-, there was a slowly developing but marked depolarization. 4. In the absence of C1-, there was an early depolarization which increased in high-PCO2 or low-K+ solutions, and decreased in low-PCO2, high-K+ or Na+-free solutions. Changing the HCO3- concentration did not modify the depolarization. 5. The early depolarization and contractions observed in C1--free Ringer persisted in presence of tubocurarine chloride (2.5-10(-5) M/1). 6. Possible mechanisms for the depolarization are discussed.
The short-term influence of catecholamines on surface pH (pHs) and intracellular pH (pHi) of superficial muscle fibres has been investigated in rat soleus in vitro using single-barrelled and double-barrelled glass micro-electrodes. pHs means the pH recorded at the surface of a muscle fibre. All measurements were performed in high-Ca2+ (10 mM) Ringer's solutions. Adrenaline caused an intracellular and surface acidification which increased with concentration in the range 6 X 10(-9)-6 X 10(-6) M. The effect was inhibited by propranolol (10(-5)M) but not by phentolamine (1.5 X 10(-7) M). Noradrenaline and isoproterenol (6 X 10(-6) M) also acidified the intracellular fluid. The relative effect of catecholamines on steady-state pHi was: adrenaline = isoproterenol greater than noradrenaline. Adrenaline (6 X 10(-9)-6 X 10(-6) M) did not accelerate pHi recovery following intracellular acid-loading by NH+4 or CO2. It is concluded that activation of beta-adrenoceptors by catecholamines causes an early intracellular acidosis presumably by enhancing synthesis of metabolic acids. The surface acidification seems at least partly due to non-ionic permeation of sarcolemma by metabolic acids, secondarily inducing accumulation of H+ ions at the cell surface.
"The fibre water of frog skeletal muscle was increased by exposure of the muscle to CO2. Exposure to acid at constant PCO2 caused no change in fibre water although muscle weight decreased, whereas exposure to alkali increased fibre water.
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