Interaction of external H+ with the Na+-H+ exchanger in renal microvillus membrane vesicles.

Aronson, Peter S.; Suhm, M A; Nee, J. J.

doi:10.1016/s0021-9258(18)32287-7

Cited by 194 publications

(17 citation statements)

References 18 publications

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“…(1) the 13% CO 2 -induced acidification was too small; (2) there was no change in the proton gradient across the Na/H exchanger; and (3) the 13% CO 2 -equilibrated Ringer is acidic relative to control (pH 7.09 vs. 7.5), and the low extracellular pH may have inhibited the Na/H exchanger (Aronson et al, 1983). We ruled out the first possibility with a 10-mM NH 4 prepulse that caused only ≈0.1 decrease in pH i (n = 4) but still showed the characteristic Na/H exchanger-mediated pH i recovery; in comparison, 13% apical CO 2 acidified the cell by >0.2 pH units.…”

Section: Basolateral Membrane Hco 3 Transportersmentioning

confidence: 99%

CO2-induced ion and fluid transport in human retinal pigment epithelium

Adijanto

Banzon

Jalickee

et al. 2009

Journal of General Physiology

116

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In the intact eye, the transition from light to dark alters pH, [Ca2+], and [K] in the subretinal space (SRS) separating the photoreceptor outer segments and the apical membrane of the retinal pigment epithelium (RPE). In addition to these changes, oxygen consumption in the retina increases with a concomitant release of CO2 and H2O into the SRS. The RPE maintains SRS pH and volume homeostasis by transporting these metabolic byproducts to the choroidal blood supply. In vitro, we mimicked the transition from light to dark by increasing apical bath CO2 from 5 to 13%; this maneuver decreased cell pH from 7.37 ± 0.05 to 7.14 ± 0.06 (n = 13). Our analysis of native and cultured fetal human RPE shows that the apical membrane is significantly more permeable (≈10-fold; n = 7) to CO2 than the basolateral membrane, perhaps due to its larger exposed surface area. The limited CO2 diffusion at the basolateral membrane promotes carbonic anhydrase–mediated HCO3 transport by a basolateral membrane Na/nHCO3 cotransporter. The activity of this transporter was increased by elevating apical bath CO2 and was reduced by dorzolamide. Increasing apical bath CO2 also increased intracellular Na from 15.7 ± 3.3 to 24.0 ± 5.3 mM (n = 6; P < 0.05) by increasing apical membrane Na uptake. The CO2-induced acidification also inhibited the basolateral membrane Cl/HCO3 exchanger and increased net steady-state fluid absorption from 2.8 ± 1.6 to 6.7 ± 2.3 µl × cm−2 × hr−1 (n = 5; P < 0.05). The present experiments show how the RPE can accommodate the increased retinal production of CO2 and H2O in the dark, thus preventing acidosis in the SRS. This homeostatic process would preserve the close anatomical relationship between photoreceptor outer segments and RPE in the dark and light, thus protecting the health of the photoreceptors.

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Section: Basolateral Membrane Hco 3 Transportersmentioning

confidence: 99%

CO2-induced ion and fluid transport in human retinal pigment epithelium

Adijanto

Banzon

Jalickee

et al. 2009

Journal of General Physiology

116

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“…External pH (pH.) Dependence Na,'/H, exchange in a variety of cells, including thymocytes, is inhibited by Ho (Rindler and Saier, 1981 ;Aronson, 1983;Aronson et al, 1983;Grinstein et al ., 1984x), at least partly by competition with Nao for the externally facing binding site . Thus, a change in the inhibitory potency of W tbuld conceivably result in activation of forward (Na'/H ;) exchange .…”

Section: Activation Of Exchange As a Function Of Medium Osmolaritymentioning

confidence: 99%

Mechanism of osmotic activation of Na+/H+ exchange in rat thymic lymphocytes.

Grinstein¹,

Rothstein²,

Cohen³

1985

The Journal of General Physiology

155

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The activity of the Na'/H' exchange system of rat thymic lymphocytes was determined by means of intracellular (pHi) and extracellular pH (pH.) measurements . In isotonic media, the antiport is virtually quiescent at physiological pHi (7 .0-7 .1), but is greatly activated by cytoplasmic acidification . At normal pH i, the antiport can also be activated by osmotic shrinking. Osmotic activation occurs after a delay of 20-30 s and is reversed several minutes after iso-osmolarity is restored . The mechanism of activation was analyzed by comparing the kinetic parameters of transport in resting (isotonic) and hyperosmotically stressed cells. The affinities of the external substrate site for Na' and H+ are not altered in shrunken cells. In contrast, the H; sensitivity of the antiport (which is largely dictated by an allosteric modifier site) was increased, which accounted for the activation . The concentration of free cytoplasmic Ca" ([Ca 2+ ];) increased after osmotic shrinking. This increase was dependent on the presence of extracellular Ca" and Na' and was blocked by inhibitors of Na'/H' exchange, which suggests that it is a consequence, rather than the cause, of the activation of the antiport . It is concluded that the shift in the pHi dependence of the modifier site of the Na'/H' antiport is the primary event underlying the regulatory volume increase that follows osmotic shrinkage.

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“…The lack of efficacy of K t, Rb t, and Cs t appears to relate to the carrier's being devoid of affinity, or nearly so, for these ions. Thus, the order of relative affinities is Li t > Na t >> K § Rb t, Cs t, a relationship that is also obtained in rabbit renal proximal tubule cells Aronson, 1980, 1981a;Burnham et al, 1982;Aronson, 1983;Aronson et al, 1983), mouse neuroblastoma cells (Moolenaar et al, 1981), hamster lung fibroblasts (Paris and Pouyss6gur, 1983;L'Allemain et al, 1984b), and rat thymic lymphocytes .…”

Section: Kinetic Propertiesmentioning

confidence: 57%

“…Ion selectivity. The Km for external Na +, one of the physiologically relevant substrates, is ~21 mM, a value that can be compared with the range of 5-59 mM reported for rabbit renal proximal tubule vesicles (Kinseila and Aronson, 1981b;Warnock et al, 1982;Burnham et al, 1982;Aronson et al, 1983), cultured dog kidney cells (Rindler et al, 1979), rat thymocytes , human A431 epidermoid carcinoma cells (Rothenberg et al, 1983), hamster pulmonary fibroblasts (Paris and Pouyss6gur, 1983;L'Allemain et al, 1984b), mouse neuroblastoma cells (Moolenaar et al, 1981), and chick myoblasts (Vigne et al, 1982). Apparently, like a variety of other cell types (Rindler et al, 1979;Moolenaar et al, 1981;Burnham et al, 1982;Aronson, 1983;Paris and Pouyss6gur, 1983), Li + may serve as an effective substitute for Na +, albeit with an even slightly higher affinity (Kin -14 mM), whereas K t, Rb t, and Cs § cannot replace Na t (Kinsella and Aronson, 1980;Burnham et al, 1982;Aronson, 1983;.…”

Section: Kinetic Propertiesmentioning

confidence: 79%

“…Apparently, like a variety of other cell types (Rindler et al, 1979;Moolenaar et al, 1981;Burnham et al, 1982;Aronson, 1983;Paris and Pouyss6gur, 1983), Li + may serve as an effective substitute for Na +, albeit with an even slightly higher affinity (Kin -14 mM), whereas K t, Rb t, and Cs § cannot replace Na t (Kinsella and Aronson, 1980;Burnham et al, 1982;Aronson, 1983;. In other cells, including rabbit brush border vesicles (Kinsella and Aronson, 198 la;Burnham et al, 1982;Aronson, 1983;Aronson et al, 1983), dog kidney cells (Rindler et al, 1979), and hamster lung fibroblasts (Paris and Pouyss6gur, 1983), apparent Km values of 1-12 mM for Li t have been reported. However, the transport rate for Li t across the neutrophil cell membrane is twofold slower than for Na t, similar to the findings in rabbit renal tubules (Kinsella and Aronson,198 l a), rat thymocytes , and hamster lung fibroblasts (L'Allemain et al, 1984b).…”

Section: Kinetic Propertiesmentioning

confidence: 99%

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Intracellular acidification-induced alkali metal cation/H+ exchange in human neutrophils.

Simchowitz

Cragoe

1987

The Journal of General Physiology

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Pretreatment of isolated human neutrophils (resting pHi -~ 7.25 at pHo 7.40) with 30 mM NH4CI for 30 min leads to an intracellular acidification (pHi ~ 6.60) when the NH4CI prepulse is removed. Thereafter, in 140 mM Na + medium, pHi recovers exponentially with time (initial rate, -0.12 pH/min) to reach the normal resting pHi by -20 rain, a process that is accomplished mainly, if not exclusively, though an exchange of internal H + for external Na +. This Na+/H + countertransport is stimulated by external Na + (Km ~' 21 mM) and by external Li + (Km ~' 14 raM), though the maximal transport rate for Na + is about twice that for Li +. Both Na + and Li + compete as substrates for the same translocation sites on the exchange carrier. Other alkali metal cations, such as K +, Rb +, or Cs +, do not promote pHi recovery, owing to an apparent lack of affinity for the carrier. The exchange system is unaffected by ouabain or furosemide, but can be competitively inhibited by the diuretic amiloride (Ki 8 ~M). The influx of Na + or Li + is accompanied by an equivalent counterefflux of H +, indicating a 1:1 stoichiometry for the exchange reaction, a finding consistent with the lack of voltage sensitivity (i.e., electroneutrality) of pHi recovery. These studies indicate that the predominant mechanism in human neutrophils for pHi regulation after intracellular acidiftcation is an amiloridesensitive alkali metal cation/H + exchange that shares a number of important features with similar recovery processes in a variety of other mammalian cell types.

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Interaction of external H+ with the Na+-H+ exchanger in renal microvillus membrane vesicles.

Cited by 194 publications

References 18 publications

CO2-induced ion and fluid transport in human retinal pigment epithelium

CO2-induced ion and fluid transport in human retinal pigment epithelium

Mechanism of osmotic activation of Na+/H+ exchange in rat thymic lymphocytes.

Intracellular acidification-induced alkali metal cation/H+ exchange in human neutrophils.

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