Influence of extracellular pH and perfusion rate on Na+/H+ exchange in cultured opossum kidney cells

Gennari, F. John; Helmle-Kolb, Corinna; Murer, Heini

doi:10.1007/bf00374984

Cited by 8 publications

(3 citation statements)

References 12 publications

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“…A second focus might be the kinetic basis for enhancement of antiporter flux with axial flow. Gennari, Helmle-Kolb, and Murer (1992) observed an increase in antiporter flux in QK cells when superfusion rates were increased, and they could discern no gross change in Na + affinity, KNa. With reference to Eq.…”

Section: Discussionmentioning

confidence: 93%

A kinetically defined Na+/H+ antiporter within a mathematical model of the rat proximal tubule.

1995

The Journal of General Physiology

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The luminal membrane antiporter of the proximal tubule has been represented using the kinetic formulation of E. Heinz (1978, . The membrane density of the antiporter was selected to yield agreement with the rate of tubular Na + reabsorption. Simulation of 0.5 cm of tubule predicts that the activity of the Na+/H + antiporter is the most important force for active secretion of ammonia. Model calculations of metabolic acid-base disturbances are performed and comparison is made among antiporter representations (kinetic model, kinetic model without internal modifier, and NET formulation). It is found that the ability to sharply turn off Na+/H + exchange in cellular alkalosis substantially eliminates the cell volume increase associated with high HCO~ conditions. In the tubule model, diminished Na+/H + exchange in alkalosis blunts the axial decrease in luminal HCO~ and thus diminishes paracellular reabsorption of CI-. In this way, the kinetics of the Na+/H + antiporter could act to enhance distal delivery of Na § CI-, and HCO~ in acute metabolic alkalosis.

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Section: Discussionmentioning

confidence: 93%

A kinetically defined Na+/H+ antiporter within a mathematical model of the rat proximal tubule.

1995

The Journal of General Physiology

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“…Primary myocytes cultures were shown to respond to low external pH by increasing NHE1 protein expression (Rehring et al, 1998). Likewise, cells derived from renal epithelia respond to extracellular acidity by increasing NHE1 levels (Moe et al, 1991;Gennari et al, 1992;Rutherford et al, 1997). But not all cells upregulate NHE1 in response to extracellular acidity.…”

Section: Discussionmentioning

confidence: 98%

Extracellular pH Controls NHE1 Expression in Epidermis and Keratinocytes: Implications for Barrier Repair

Hachem

Behne

Aronchik

et al. 2005

Journal of Investigative Dermatology

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We have previously shown that the Na+/H+ antiporter (NHE1) is an essential endogenous pathway responsible for stratum corneum (SC) acidification. Since the epidermis must re-establish its epidermal barrier after acute barrier perturbations, we asked whether the NHE1 was, in turn, regulated by changes in barrier status. We found that in vivo epidermal NHE1 expression was upregulated within hours of barrier disruption. We next asked whether NHE1 was regulated by barrier status per se, or by the SC alkalinization that accompanies barrier perturbation. NHE1 was upregulated by alkalinizing SC pH, whereas this antiporter was downregulated by acidifying SC pH, independent of changes in barrier status. Moreover, acidifying SC pH overrode the effects of barrier break in regulating NHE1 expression, suggesting that SC alkalinization is the major stimulus for increased NHE1 expression. Finally, we confirmed that the keratinocyte NHE1 antiporter is regulated by extracellular pH independent of barrier status, by demonstrating that NHE1 was upregulated in cultured keratinocytes exposed to pH 8.3 medium and downregulated in cultured keratinocytes exposed to pH 6.3 medium. These data suggest that the keratinocyte NHE1 is regulated by extracellular pH. SC barrier break also upregulates NHE1 expression, but this response seems to be mediated by concomitant changes in SC pH.

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“…It is well established that NaHCO 3 reabsorption in the proximal tubule increases in response to an increase in axial flow rate due to flow-dependent stimulation of Na ϩ /H ϩ antiporter activity (43). Perfusion rate has also been shown to modulate Na ϩ /H ϩ exchange and the rate of H ϩ secretion in cultured opossum kidney cells (19). Flow dependence of solute reabsorption in the proximal tubule, with its apical brush- border membrane, has been attributed to flow rateinduced alterations in concentration gradients in the vicinity of the apical membrane.…”

Section: Discussionmentioning

confidence: 99%

Epithelial Na⁺ channels are regulated by flow

Satlin

Sheng

Woda

et al. 2001

American Journal of Physiology-Renal Physiology

198

167

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Na(+) absorption in the renal cortical collecting duct (CCD) is mediated by apical epithelial Na(+) channels (ENaCs). The CCD is subject to continuous variations in intraluminal flow rate that we speculate alters hydrostatic pressure, membrane stretch, and shear stress. Although ENaCs share limited sequence homology with putative mechanosensitive ion channels in Caenorhabditis elegans, controversy exists as to whether ENaCs are regulated by biomechanical forces. We examined the effect of varying the rate of fluid flow on whole cell Na(+) currents (I(Na)) in oocytes expressing mouse alpha,beta,gamma-ENaC (mENaC) and on net Na(+) absorption in microperfused rabbit CCDs. Oocytes injected with mENaC but not water responded to the initiation of superfusate flow (to 4-6 ml/min) with a reversible threefold stimulation of I(Na) without a change in reversal potential. The increase in I(Na) was variable among oocytes. CCDs responded to a threefold increase in rate of luminal flow with a twofold increase in the rate of net Na(+) absorption. An increase in luminal viscosity achieved by addition of 5% dextran to the luminal perfusate did not alter the rate of net Na(+) absorption, suggesting that shear stress does not influence Na(+) transport in the CCD. In sum, our data suggest that flow stimulation of ENaC activity and Na(+) absorption is mediated by an increase in hydrostatic pressure and/or membrane stretch. We propose that intraluminal flow rate may be an important regulator of channel activity in the CCD.

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Influence of extracellular pH and perfusion rate on Na+/H+ exchange in cultured opossum kidney cells

Cited by 8 publications

References 12 publications

A kinetically defined Na+/H+ antiporter within a mathematical model of the rat proximal tubule.

A kinetically defined Na+/H+ antiporter within a mathematical model of the rat proximal tubule.

Extracellular pH Controls NHE1 Expression in Epidermis and Keratinocytes: Implications for Barrier Repair

Epithelial Na⁺ channels are regulated by flow

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Influence of extracellular pH and perfusion rate on Na+/H+ exchange in cultured opossum kidney cells

Cited by 8 publications

References 12 publications

A kinetically defined Na+/H+ antiporter within a mathematical model of the rat proximal tubule.

A kinetically defined Na+/H+ antiporter within a mathematical model of the rat proximal tubule.

Extracellular pH Controls NHE1 Expression in Epidermis and Keratinocytes: Implications for Barrier Repair

Epithelial Na+ channels are regulated by flow

Contact Info

Product

Resources

About

Epithelial Na⁺ channels are regulated by flow