pH regulation in barnacle muscle fibers: dependence on extracellular sodium and bicarbonate

Boron, Walter F.; McCormick, W. C.; Roos, Albert de

doi:10.1152/ajpcell.1981.240.1.c80

Cited by 109 publications

(67 citation statements)

References 10 publications

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“…The half-time for the decrease in at1 immediately after reintroduction of C02/HCO3 was 1-79±0-16 (n = 18, measured during the first 4 min). (Boron, McCormick & Roos, 1981;Moody, 1981). Consistent with this interpretation is the finding that the loss of Cl was more affected by the removal of CO2 from the superfusing solution than was the reaccumulation.…”

Section: Resultsmentioning

confidence: 56%

The role of chloride‐bicarbonate exchange in the regulation of intracellular chloride in guinea‐pig vas deferens.

Aickin¹,

Brading²

1984

The Journal of Physiology

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SUMMARY1. The Cl-depleted smooth muscle cells of guinea-pig vas deferens rapidly restore their intracellular Cl activity (ai1) to a level 5 times higher than that predicted by a passive distribution when Cl-ions are readmitted to the extracellular solution.2. Cl reaccumulation, measured using Cl-sensitive micro-electrodes and the uptake of 36CI, was slowed about 3-fold by the nominal absence of CO2 and HCO3 and about 10-fold by the presence of the anion exchange inhibitor DIDS (4-4'-diisothiocyanostilbene-2,2'-disulphonic acid). However, the usual level of intracellular Cl was eventually attained and neither condition reduced intracellular Cl in normal tissues.3. The loss of intracellular Cl that occurs when Cl-ions are removed from the extracellular solution was slowed about 3-fold by the nominal absence of CO2 and HCO3 and was accelerated by their readdition. DIDS slowed the fall in ai about 10-fold and reduced 36CI efflux.4. Intracellular pH (pHi), measured using pH-sensitive micro-electrodes, increased by a mean of 0 73 units when Cl was removed from the superfusing solution in the presence of CO2 and HCO3, and rapidly decreased when Cl was readmitted. These changes are equivalent to an intracellular accumulation and loss of HCO3-ions respectively. The net transmembrane movement of HCO3-ions which would have caused these changes in pHi was calculated using the measured intracellular buffering power (Aickin, 1984). 25% fewer HC03-ions than Cl-ions were accumulated and lost and the HCO3 movement was completed 2-3 times faster than the simultaneous Cl movement under the same conditions. 5. The changes in pHi induced by alteration of extracellular Cl were reduced by the nominal absence of CO2 and HCO3 and abolished by the presence of DIDS. The acidification recorded on readmission of Cl in the nominal absence of CO2 and HCO3 was compatible with a metabolic production of about 0-1 % CO2.6. We conclude that Cl-HCO3 exchange plays a major role in the regulation of intracellular Cl. The exchange carrier is reversible, is completely inhibited by DIDS, and accounts for about 75 % of the net Cl movement that occurs when Cl is removed from or readmitted to the extracellular solution. The mechanism which is responsible for the remaining Cl movement remains to be elucidated.

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Section: Resultsmentioning

confidence: 56%

The role of chloride‐bicarbonate exchange in the regulation of intracellular chloride in guinea‐pig vas deferens.

Aickin¹,

Brading²

1984

The Journal of Physiology

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“…In other experiments, SITS was less effective, and when we tried to make a solution containing both amiloride and SITS we obtained a precipitate. (Thomas, 1977;Boron, McCormick & Roos, 1981;Moody, 1981;Boron & Russell, 1983). When we initially tested the effects ofremoving Na on pH, recovery of leech neurones in a HC03--buffered solution, we found that some recovery still occurred.…”

Section: Leech Neurone Ph3mentioning

confidence: 99%

A dual mechanism for intracellular pH regulation by leech neurones.

Schlue¹,

Thomas²

1985

The Journal of Physiology

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SUMMARY1. Neutral-carrier pH-sensitive micro-electrodes were used to investigate intracellular pH (pHj) 4. In HC03--free solutions, pHi recovery from acidification was blocked by removing external Na or by amiloride (2 mM).5. In solutions buffered with 20 CO2 and 11 mM-HCO3-, amiloride slowed but did not block pHi recovery. The anion exchange inhibitor SITS (4-acetamido-4'-isothiocyanato-stilbene-2,2'-disulphonic acid) also slowed pHi recovery in the presence of HCO3-.6. In CO2/HCO3-solution the removal of external Na either slowed or blocked pH1recovery, and blocked it completely in the presence of amiloride.7. We conclude that in HCO3--free solutions pHi regulation is by a Na-H exchange system; but in the presence of HCO3-there is an additional mechanism which is probably a Na-dependent Cl-HCO3 exchanger.

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“…The best-characterized pHi regulatory mechanism in mammals is sodium/hydrogen (Na+/H+) exchange (1)(2)(3)(4)(5). In some cells pH, is also regulated by bicarbonate (HCO-) transport, including (a) Na+-dependent Cl-/HCO-exchange in invertebrate (6)(7)(8)(9) and also in mammalian cells (10)(11)(12)(13)(14), (b) Na+-independent This study was presented in part at the American Gastroenterological Association Meeting, New Orleans, May 1988. (1988.…”

Section: Introductionmentioning

confidence: 99%

Bicarbonate-dependent and -independent intracellular pH regulatory mechanisms in rat hepatocytes. Evidence for Na+-HCO3- cotransport.

Gleeson¹,

Smith²,

Boyer³

1989

J. Clin. Invest.

103

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Using the pH-sensitive dye 2,7-bis(carboxyethyl)-5(6)-carboxy-fluorescein and a continuously perfused subconfluent hepatocyte monolayer cell culture system, we studied rat hepatocyte intracellular pH (pH,) regulation in the presence (+HCO3) and absence (-HCO3) of bicarbonate. Baseline pH, was higher (7.28±09) in +HCO3 than in -HCO3 (7.16±0.14). Blocking Na+/H' exchange with amiloride had no effect on pH1 in +HCO3 but caused reversible 0.1-0.2-U acidification in -HCO3 or in +HCO3 after preincubation in the anion transport inhibitor 4,4'-diisothiocyano-2,2'-disulfonic acid stilbene (DIDS). Acute Na' replacement in +HCO3 also caused acidification which was amiloride independent but DIDS inhibitible.The recovery of pH, from an intracellular acid load (maximum H+ efilux rate) was 50% higher in +HCO3 than in -HCO3. Amiloride inhibited H+ efflux..M by 75% in -HCOj but by only 27% in +HCO3. The amiloride-independent pH, recovery in +HCO3 was inhibited 50-63% by DIDS and 79% by Na+ replacement but was unaffected by depletion of intracellular Cl-, suggesting that Cl-/HCO3 exchange is not involved. Depolarization of hepatocytes (raising external K+ from 5 to 25 mM) caused reversible 0.05-0.1-U alkalinization, which, however, was neither Na+ nor HCO3 dependent, nor DIDS inhibitible, findings consistent with electroneutral HCO3 transport.We conclude that Na'-HCO3 cotransport, in addition to Na+/H+ exchange, is an important regulator of pH1 in rat hepatocytes.

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pH regulation in barnacle muscle fibers: dependence on extracellular sodium and bicarbonate

Cited by 109 publications

References 10 publications

The role of chloride‐bicarbonate exchange in the regulation of intracellular chloride in guinea‐pig vas deferens.

The role of chloride‐bicarbonate exchange in the regulation of intracellular chloride in guinea‐pig vas deferens.

A dual mechanism for intracellular pH regulation by leech neurones.

Bicarbonate-dependent and -independent intracellular pH regulatory mechanisms in rat hepatocytes. Evidence for Na+-HCO3- cotransport.

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