Na-HCO3 cotransport and Na-H antiporter in chronic respiratory acidosis and alkalosis

Ruiz, Ofelia S.; Arruda, José A.L.; Talor, Zvi

doi:10.1152/ajprenal.1989.256.3.f414

Cited by 32 publications

(37 citation statements)

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“…Parallel modulation of apical and basolateral membrane H+/OH-/HCO transporters in response to a variety of conditions has been extensively documented in the proximal tubule. Parallel adaptive increases in apical membrane Na+/H+ antiporter activity and basolateral membrane Na+/3HCO5 cotransporter activity have been found under the chronic conditions of metabolic acidosis (35,36) and alkalosis (35), respiratory acidosis (37,38) and alkalosis (37), hyperfiltration (39), and K+ depletion (40). In addition, acute exposure of the in vitro microperfused proximal tubule to angiotensin II has been found to increase in parallel the activities of these two transporters (41 ).…”

Section: Discussionmentioning

confidence: 85%

Mineralocorticoid modulation of apical and basolateral membrane H+/OH-/HCO3- transport processes in the rabbit inner stripe of outer medullary collecting duct.

Hays

1992

J. Clin. Invest.

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To examine the mechanism by which mineralocorticoids regulate HCO3-absorption in the rabbit inner stripe of the outer medullary collecting duct, we microfluorometrically measured intracellular pH (pH1) in in vitro perfused tubules using 2',7'-bis(carboxyethyl)-5(6)-carboxyfluorescein (BCECF) assaying the apical and basolateral membrane H'/OH-/HCO3 (control, 72.7±15.7 pmol -mm-' * min-vs DOCA, 132.3±22.5 pmol. mm-1 min-', P < 0.02), while the K112 for Cl-was unchanged. Basolateral membrane Na+/H+ antiporter activity assayed as the Na+-dependent pH1 recovery from an acid load was not changed in chronic DOCA tubules versus controls. In conclusion, the apical membrane H+ pump and basolateral membrane Cl-/HCO3 exchanger of the rabbit OMCDI are regulated in parallel without chronic alterations in pH1 under the conditions of mineralocorticoid excess and deficiency. The parallel changes in these transporters accounts for the alterations in OMCDj HCO3 absorption seen under these condi-

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Section: Discussionmentioning

confidence: 85%

Mineralocorticoid modulation of apical and basolateral membrane H+/OH-/HCO3- transport processes in the rabbit inner stripe of outer medullary collecting duct.

Hays

1992

J. Clin. Invest.

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“…Sci. USA 87 (1990) also been found by some investigators to cause an increase in Na/H antiporter activity (15)(16)(17). In the next series of studies, we performed experiments similar to those described above, with the exception that acid medium was identical to control medium, and acid cells were placed in a 10% C02/ 90% air incubator while control cells were placed in a 5% C02/95% air incubator.…”

mentioning

confidence: 87%

Preincubation in acid medium increases Na/H antiporter activity in cultured renal proximal tubule cells.

Horie

Moe

Tejedor

et al. 1990

Proc. Natl. Acad. Sci. U.S.A.

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Chronic acidosis in vivo leads to an increase in proximal tubule Na/H antiporter activity that persists when the transporter is studied out of the acidotic environment. It is presently not clear whether a decrease in extracellular fluid pH alone is sufficient to elicit this adaptation. The present studies examined the effect of acid preincubation on Na/H antiporter activity in cultured proximal tubule cells. Antiporter activity was examined after a 2-day preincubation in control or acid medium, 1 hr after removal from the preincubation fluid.Na/H antiporter activity was assayed as the initial rate of (vol/vol) to the culture medium for the first 3 days to allow better cell attachment. After achieving confluence (8-12 days), cells were rendered quiescent by removal of insulin and hydrocortisone for 48 hr prior to and during preincubation (10).Cultured fibroblasts were derived from human foreskin and used in passages 5-7 (11). Fibroblasts were grown on glass coverslips in DMEM supplemented with penicillin (100 units/ ml), streptomycin (100 ,ug/ml), and 10% fetal bovine serum. Fibroblasts were incubated with a reduced concentration of fetal bovine serum (1%) for 24 hr prior to and during preincubation.Measurement of Intracellular pH and Na/H Antiporter Activity. Continuous measurement of cytoplasmic pH (pHi) was accomplished using the intracellularly trapped pHsensitive dye 2',7'-bis(2-carboxyethyl)-5-(and -6)carboxyfluorescein (BCECF acid). Cells were loaded with the acetoxymethyl ester of BCECF (10 ,uM)

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“…A number of chronic conditions associated with increased proximal tubular H secretory capacity, including chronic metabolic and respiratory acidosis, chronic K deficiency, and chronic hyperfiltration, are all associated with adaptations in proximal tubular function (2)(3)(4)(5)(6)(7)(8)(9)(10)(11)(12)(13)(14)(15)(16). These adaptations include increased activities ofthe apical membrane Na/H antiporter and Na/citrate cotransporter, the basolateral membrane Na/3HCO3 cotransporter, phosphatedependent glutaminase, and phosphoenolpyruvate carboxykinase (2)(3)(4)(5)(6)(7)(8)(9)(10)(11)(12)(13)(14). A common feature of these proteins is that they all contribute to net acid excretion, either through acid secretion or ammonia synthesis.…”

Section: Introductionmentioning

confidence: 99%

“…Kinetic studies on the transporters have found that substrate affinities are unaffected and Vm. is increased (3,6,8,9,11).…”

Section: Introductionmentioning

confidence: 99%

Long-term activation of protein kinase c causes chronic Na/H antiporter stimulation in cultured proximal tubule cells.

Horie¹,

Moe²,

Miller³

et al. 1992

J. Clin. Invest.

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To examine the role of protein kinase C as a chronic regulator of proximal tubule Na/H antiporter activity, the effect of phorbol 12-myristate 13-acetate (PMA) on the Na/H antiporter was studied in cultured proximal tubule cells. Short-term activation of protein kinase C by 5 min exposure to PMA caused an acute increase in Na/H antiporter activity that was not prevented by cycloheximide or actinomycin D and did not persist 24 h later. Long-term activation of protein kinase C by 2 h exposure to PMA caused a dose-dependent increase in Na/H antiporter activity 24 h later. This latter effect was due to protein kinase C activation in that it was inhibited by sphingosine and was not seen with 4a-PMA, an inactive analogue. The chronic effect of PMA was inhibited by 10 nM actinomycin D or 7 ,uM cycloheximide. Proximal tubule cells exposed to PMA for 2 h demonstrated a two-to threefold increase in Na/H antiporter mRNA (mRNAN,/H) abundance 4 h later. In conclusion, short-term activation of protein kinase C leads to a transient increase in Na/H antiporter activity that is independent of transcription and translation, whereas long-term activation of protein kinase C causes a persistent increase in antiporter activity that is dependent on transcription and translation and is associated with increased mRNAN,/H abundance. This latter effect may mediate increased Na/H antiporter activity in a number of chronic conditions. (J. Clin. Invest. 1992. 89:365-372.)

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Na-HCO3 cotransport and Na-H antiporter in chronic respiratory acidosis and alkalosis

Cited by 32 publications

References 0 publications

Mineralocorticoid modulation of apical and basolateral membrane H+/OH-/HCO3- transport processes in the rabbit inner stripe of outer medullary collecting duct.

Mineralocorticoid modulation of apical and basolateral membrane H+/OH-/HCO3- transport processes in the rabbit inner stripe of outer medullary collecting duct.

Preincubation in acid medium increases Na/H antiporter activity in cultured renal proximal tubule cells.

Long-term activation of protein kinase c causes chronic Na/H antiporter stimulation in cultured proximal tubule cells.

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