Surface pH and the control of intracellular pH in cardiac and skeletal muscle

Hemptinne, Alexandre de; Marrannes, Roger; Vanheel, Bert

doi:10.1139/y87-154

Cited by 46 publications

(39 citation statements)

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“…Several studies have provided histochemical (Ridderstråle, 1979;Lönnerholm, 1980;Riley et al 1982;Dermietzel et al 1985;Decker et al 1996), biochemical (Wetzel & Gros, 1990 and functional evidence (Zborowska-Sluis et al 1974;Effros & Weissman, 1979;Geers et al 1985;De Hemptinne et al 1987) for a membrane-bound, sarcolemmal carbonic anhydrase (CA) in skeletal muscle. Waheed et al (1992) have demonstrated that in rat skeletal muscle the sarcolemmal CA is a 39 kDa, glycosylated, phosphatidylinositol-glycan anchored CA IV.…”

Section: _1mentioning

confidence: 99%

Extracellular carbonic anhydrase activity facilitates lactic acid transport in rat skeletal muscle fibres

Wetzel

Hasse

Papadopoulos

et al. 2001

The Journal of Physiology

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1. In skeletal muscle an extracellular sarcolemmal carbonic anhydrase (CA) has been demonstrated. We speculate that this CA accelerates the interstitial CO 2 /HCO 3 _ buffer system so that H + ions can be rapidly delivered or buffered in the interstitial fluid. Because > 80 % of the lactate which crosses the sarcolemmal membrane is transported by the H + -lactate cotransporter, we examined the contributions of extracellular and intracellular CA to lactic acid transport, using ion-selective microelectrodes for measurements of intracellular pH (pH i ) and fibre surface pH (pH s ) in rat extensor digitorum longus (EDL) and soleus fibres.2. Muscle fibres were exposed to 20 mM sodium lactate in the absence and presence of the CA inhibitors benzolamide (BZ), acetazolamide (AZ), chlorzolamide (CZ) and ethoxzolamide (EZ The membrane-permeable CA inhibitors CZ (0.5 mM) and EZ (0.1 mM), which inhibit the extracellular as well as the intracellular CAs, exerted no greater effects than the poorly permeable inhibitors BZ and AZ did.6. In soleus, 10 mM cinnamate inhibited the lactate influx by 47 %. Addition of 0.01 mM BZ led to a further inhibition by only 10 %. BZ alone reduced the influx by 37 %.7. BZ (0.01 mM) had no influence on the K m value of the lactate transport, but led to a decrease in maximal transport rate (V max ). In EDL, BZ reduced V max by 50 % and in soleus by about 25 %.8. We conclude that the extracellular sarcolemmal CA plays an important role in lactic acid transport, while internal CA has no effect, a difference most likely attributable to the high internal vs. low extracellular BF non-HCO 3 . The fact that the effects of cinnamate and BZ are not additive indicates that the two inhibitors act at distinct sites on the same transport pathway for lactic acid.

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Section: _1mentioning

confidence: 99%

Extracellular carbonic anhydrase activity facilitates lactic acid transport in rat skeletal muscle fibres

Wetzel

Hasse

Papadopoulos

et al. 2001

The Journal of Physiology

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“…Finally, it is worth considering whether alteration of the extracellular buffering capacity and hence of the pH at the immediate surface of the preparation influences the pH, transients and steady-state values in the presence and nominal absence of C02-HCO3-(see de Hemptinne, Morranne & Vanheel, 1987). Increased intracellular acid loading and hence acid extrusion in the nominal absence of C02-HCO3-may lead to a lower surface pH and hence contribute to the slower recovery and lower steady-state pHi.…”

Section: Na+-h+ Exchangementioning

confidence: 99%

Regulation of intracellular pH in the smooth muscle of guinea‐pig ureter: Na+ dependence.

Aickin¹

1994

The Journal of Physiology

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1. Mechanisms involved in the regulation of intracellular pH (pHi) in smooth muscle cells of guinea-pig ureter have been investigated using double-barrelled pH-sensitive microelectrodes in isolated strips of tissue. 2. Removal of C02-HC03-from the superfusing solution caused a fall in the steady-state pH, except in a few cells which had been excised from the animal for many hours (usually >24 h). The pHi value was 7-22 + 0 09 (n = 89; mean + S.D. of an observation) in solution buffered with 5% CO2-21 mm HC03-, compared with 6-92 + 024 (n = 67) in the nominal absence of CO2-HCO3-. Recovery from experimentally induced acidosis was faster in the presence, rather than nominal absence, of C02-HC03-(mean halftimes of 2X7 + 0 7 min, n = 41, and 4X6 + 1-3 min, n = 12, respectively). These results suggest the presence of both HC03--dependent and -independent mechanisms for the effective extrusion of acid equivalents.3. Recovery from acidosis was dependent on external Na+ (Na+) in both the presence and nominal absence of C02-HCO3-, with an apparent half-maximal activation at approximately 4 and 20 mm Na+, respectively. Removal of Na' in the steady state caused a fall in pHi which proceeded at a faster rate in the presence rather than in the nominal absence of C02-HCO37-4. Amiloride (100 /uM-1 mM) reversibly inhibited the recovery from acidosis and caused a fall in the steady-state pHi when applied in the nominal absence of C02-HC03-, but had no measurable effect on either the recovery from acidosis or steady-state pHi in the presence of CO2-HCO3-. These results suggest that Na+-H+ exchange was responsible for extrusion of acid equivalents in the nominal absence of CO2 and HCO3-, but that it played little part under more physiological conditions.

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“…15 - 16 It is a routine finding even in normal well-superfused tissue and is due to the inability of diffusion and extracellular buffers to control pH in the presence of this continuing efflux of acid equivalents. 17 It is known to vary directly with the size of the preparation and the metabolic rate and to vary inversely with the external pH buffer capacity. 16 - 17 The measurement is useful in that changes in pH, can indicate changes in the cell metabolism.…”

Section: Dresdner Et Al Canine Purklnje Cell Ph After Myocardial Infamentioning

confidence: 99%

“…16 - 17 The measurement is useful in that changes in pH, can indicate changes in the cell metabolism. 17 - 18 However, it is also a required measurement for the calculation of the true transmembrane H + gradient, which cannot be determined from the difference in pH| and the bath pH (pH b ) alone.…”

Section: Dresdner Et Al Canine Purklnje Cell Ph After Myocardial Infamentioning

confidence: 99%

Intracellular pH of canine subendocardial Purkinje cells surviving in 1-day-old myocardial infarcts.

Dresdner

Kline

Wit

1989

Circulation Research

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A large reduction of intracellular potassium activity in depolarized subendocardial Purkinje fibers 24 hours after coronary artery ligation is accompanied by a much smaller increase in intracellular sodium activity. Similar intracellular ionic changes also occur during acute ischemia in ventricular muscle and are consistent with mechanisms based on intracellular acidification, which is known to occur in acutely ischemic muscle. To determine if canine subendocardial Purkinje cells 24 hours after myocardial infarction are also acidic, their intracellular pH, surface pH, and maximum diastolic potential (MDP) were measured with double-barrel pH-sensitive microelectrodes and compared with control fibers in noninfarcted hearts. In 12 mM bicarbonate Tyrode's solution (5% CO 2 -95% Oj), the average intracellular pH was not significantly different Supported by Program Project Grant HL-30557 and Grant RO1-HL31393 from National Institutes of Health, National Heart, Lung, and Blood Institute, an Irma Hirschl Career Scientist Award to R.P.K., and Postdoctoral Training Award HL-0727-08 to K.P.D.Address for correspondence: Karl P. Dresdner Jr., Department of Pharmacology, College of Physicians and Surgeons, 630 West 168th Street, New York, NY 10032.Received August 5, 1987; accepted February 21, 1989. tion, which has been shown to induce a nearly equal change in aKj and aNa,. 3 An alternative mechanism, which is also consistent with maintenance of intracellular electroneutrality, involves intracellular acidification.4 -6 If cytoplasmic proteins are the principal intracellular H+ buffers, intracellular acidification that occurs during acute ischemia 2 -7 might neutralize these buffers. The intracellular K + loosely associated with them would then be free to associate with membrane-permeable mobile anions (e.g., lactate and phosphate) and leave the cell.-The electrophysiological properties of subendocardial Purkinje cells surviving in canine infarcts 1 day after coronary artery ligation are altered by prolonged ischemia. These cells, like acutely ischemic cells, have large reductions in maximum diastolic potential (MDP) 9 -12 and significant reduction of aKj, but only a small increase in aNa,.9 One purpose of this study, therefore, was to measure the intracellular pH (pHO in these cells to determine whether it was acidic, as in acutely ischemic muscle, and

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Surface pH and the control of intracellular pH in cardiac and skeletal muscle

Cited by 46 publications

References 0 publications

Extracellular carbonic anhydrase activity facilitates lactic acid transport in rat skeletal muscle fibres

Extracellular carbonic anhydrase activity facilitates lactic acid transport in rat skeletal muscle fibres

Regulation of intracellular pH in the smooth muscle of guinea‐pig ureter: Na+ dependence.

Intracellular pH of canine subendocardial Purkinje cells surviving in 1-day-old myocardial infarcts.

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