Intracellular pH dependence of buffer capacity and anion exchange in the parietal cell

1989 ◽  
Vol 257 (5) ◽  
pp. G741-G747 ◽  
Author(s):  
E. Wenzl ◽  
T. E. Machen
Keyword(s):  
Anion Exchange ◽  
Intracellular Ph ◽  
Anion Exchanger ◽  
Buffer Capacity ◽  
Ph Dependence ◽  
Disulfonic Acid ◽  
Rates Of Change ◽  
Ethanesulfonic Acid ◽  
Increased Activity ◽  
Stimulation Of

When parietal cells (PC) are stimulated with histamine, the anion exchanger rate increases three to five times to compensate for alkaline loading induced by H+-K+ adenosinetriphosphatase (ATPase) and to provide Cl for acid secretion. It has been hypothesized that this increased activity is caused by the increase in intracellular pH (pHi) that often occurs in stimulated PC (from 7.1 to a maximum of 7.3). The dependence of the anion exchanger on pHi was studied using microspectrofluorimetry of the pH-sensitive dye 2',7'-bis(carboxyethyl)-5(6)-carboxyfluorescein (BCECF). N-2-hydroxyethylpiperazine-N'-2-ethanesulfonic acid (HEPES)-buffered solutions were used because the anion exchanger can transport OH- (or HCO3) in exchange for Cl- even with [HCO3]o = 200 microM. It was found that when solutions were changed either from NaCl to Cl- free or Cl- free to NaCl, rates of change of pHi (delta pH/delta t) were strongly dependent on pHi: nearly 0 at pHi 6.6 and 1.25 pH/min at pHi 8.0. To convert these pHi changes into anion flux rates, the intrinsic buffer capacity (beta i) was determined over the same pHi range by making small changes of [NH4]o to determine the resulting changes of [NH4]i and pHi (i.e., beta i = delta[NH4]i/delta pHi) in PC that had been pretreated with 1 mM amiloride and 200 microM [H2]4,4'-diisothiocyanostilbene-2,2'-disulfonic acid (DIDS) [to block Na+-H+ and Cl- -OH-(HCO3-) exchange]. beta i was also strongly dependent on pHi: at pHi 6.5 beta i = 48 mM/pH, and this decreased as pHi increased; at pHi 7.75 beta i = 8 mM/pH. The derived anion fluxes (i.e., JOH = beta i x delta pH/delta t) were roughly linearly related to pHi between 6.6 (JOH near 0) and 8.1 (JOH = 13 mM/min). Between pHi 7.1 and 7.3, the range normally observed during stimulation of PC, rates of anion exchange increased by 75%. This pHi sensitivity cannot explain the 300-500% increase in anion exchanger activity observed during secretagogue stimulation of PC.

Stimulation of Cl- self exchange by intracellular HCO3- in rabbit cortical collecting duct

1989 ◽  
Vol 257 (1) ◽  
pp. C94-C101 ◽  
Author(s):  
K. Matsuzaki ◽  
J. B. Stokes ◽  
V. L. Schuster
Keyword(s):  
Anion Exchange ◽  
Intracellular Ph ◽  
Rate Coefficient ◽  
Collecting Duct ◽  
Cortical Collecting Duct ◽  
High K ◽  
Shift Experiment ◽  
Ethanesulfonic Acid ◽  
The Individual ◽  
Stimulation Of

In rabbit cortical collecting duct, Cl- self exchange accounts for most of the transepithelial Cl- tracer rate coefficient, KCl (nm/s); a small fraction is effected by Cl--HCO3- exchange and Cl- diffusion. We previously reported that changing from a CO2-free N-2-hydroxyethylpiperazine-N'-2-ethanesulfonic acid (HEPES) bath to a 5% CO2-25 mM HCO3- bath stimulates Cl- self exchange. Here, we examine in further detail the individual components of the CO2-HCO3- system that stimulate KCl. Addition of 0.5% CO2 to a HEPES bath (final pH = 7.24) stimulated KCl by 70 +/- 19 nm/s, a delta KCl comparable to that induced by 1% CO2 (pH 7.12), 6% CO2 (pH 6.6), or 6% CO2-25 mM HCO3- (pH 7.4). The roles of intracellular pH (pHi) and HCO3- concentration were examined by clamping pHi using high K+ and nigericin. Increasing pHi from 6.9 to 7.6 in solutions without exogenous CO2 or HCO3- increased KCl by 71 +/- 17 nm/s. These results suggest that pHi might regulate anion exchange. However, during such a pHi-shift experiment, metabolically derived CO2 produces a concomitant change in intracellular HCO3- concentration [( HCO3-]i). To determine whether an increase in [HCO3-]i could stimulate Cl- self exchange, we replaced HEPES with 6% CO2-5 mM HCO3- isohydrically (pHi clamped at 6.9). With this increase in [HCO3-]i at constant pHi, KCl increased by 51 +/- 10 nm/s. These maneuvers had negligible effects on Cl- diffusion and Cl--HCO3- exchange. These experiments demonstrate that increases in cell [HCO3-] (or perhaps CO2) can stimulate transepithelial anion exchange.(ABSTRACT TRUNCATED AT 250 WORDS)

Basolateral Na(+)-independent Cl(-)-HCO3- exchange in primary cultures of rat IMCD cells

1992 ◽  
Vol 263 (3) ◽  
pp. F401-F410 ◽  
Author(s):  
J. A. Kraut ◽  
D. Hart ◽  
E. P. Nord
Keyword(s):  
Steady State ◽  
Cell Surface ◽  
Primary Culture ◽  
Anion Exchange ◽  
Collecting Duct ◽  
Primary Cultures ◽  
Disulfonic Acid ◽  
Absolute Requirement ◽  
Ethanesulfonic Acid ◽  
Base Load

The role of anion exchange in the regulation of intracellular pH (pHi) under base load and steady-state conditions was investigated in confluent monolayers of rat inner medullary collecting duct (IMCD) cells in primary culture using the pH-sensitive fluoroprobe 2,7-bis(carboxyethyl)-5(6')-carboxyfluorescein (BCECF). Recovery of pHi after imposition of a base load induced either by replacement of HCO3-/CO2 by N-2-hydroxyethylpiperazine-N'-2-ethanesulfonic acid (HEPES) at the same extracellular pH (pHo) or deletion of Cl- from a HCO3-/CO2-buffered solution had an absolute requirement for Cl-, was Na+ independent, and was inhibited approximately 90% by 50 microM 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid (DIDS). When pHo was decreased by lowering HCO3- concentration in the constant presence of 5% CO2, the rate of decrement in pHi was significantly blunted in the absence of Cl-. Imposition of a positive or negative diffusion potential of equal but opposite magnitude did not modify the anion exchange rate, confirming the electroneutrality of the process. Under steady-state conditions, pHi of cells bathed in a HCO3-/CO2-buffered solution was 7.33 +/- 0.06, significantly lower than that of cells bathed in a nominally HCO3-/CO2-free buffer (7.50 +/- 0.04), indicating that under physiological conditions the pathway functions as a base extruder. In studies performed on cells grown on permeable supports, the anion exchange pathway was found to be confined exclusively to the basolateral-equivalent cell surface. In summary, confluent monolayers of rat IMCD cells in primary culture possess a Na(+)-independent, DIDS-inhibitable electroneutral Cl(-)-HCO3- exchange pathway that is confined to the basolateral cell surface. The transporter is an important determinant of steady-state pHi and is the predominant mechanism whereby the cell recovers from imposed elevations in pHi.

Regulation of intracellular pH in proximal tubules of avian loopless reptilian-type nephrons

1997 ◽  
Vol 273 (6) ◽  
pp. R1845-R1854 ◽  
Author(s):  
Christina L. Martinez ◽  
Olga H. Brokl ◽  
Apichai Shuprisha ◽  
Diane E. Abbott ◽  
William H. Dantzler
Keyword(s):  
Intracellular Ph ◽  
Acid Level ◽  
Ph Sensitive ◽  
Fluorescent Dye ◽  
Proximal Tubules ◽  
Disulfonic Acid ◽  
Control Value ◽  
High K ◽  
Rate Of Recovery ◽  
Ethanesulfonic Acid

In proximal tubules isolated from chicken superficial loopless reptilian-type nephrons, intracellular pH (pHi), measured with pH-sensitive fluorescent dye 2′,7′-bis(carboxyethyl)-5(6)-carboxyfluorescein, was ∼7.1–7.2 under control conditions ( N-2-hydroxyethylpiperazine- N′-2-ethanesulfonic acid-buffered medium with pH 7.4 at 37°C), and was reduced to ∼6.9 in response to NH4Cl pulse. The rate of recovery of pHi(control value ≅ 5 × 10−3 pH U/s) from this acid level was 1) significantly decreased by removal of Na+ or both Na+ and Cl− from the bath or addition of 4,4′-diisothiocyanostilbene-2,2′-disulfonic acid (0.25 mM) to the bath, 2) significantly increased by high bath K+ (75 mM), and 3) unchanged by removal of Cl− alone from the bath or addition of ethylisopropylamiloride (1 mM) or Ba2+ (5 mM) to the bath. Resting pHi was 1) significantly decreased by Na+ or simultaneous Na+ and Cl− removal, 2) significantly increased by high K+, and 3) unchanged by Cl− removal alone or addition of Ba2+. The data do not fit the concept of pHi regulation by the most commonly suggested basolateral transporters (Na+/H+exchanger, Na+-dependent and Na+-independent Cl−/[Formula: see text]exchangers, or Na+-[Formula: see text]-[Formula: see text]cotransporter).

Control of intracellular pH during regulatory volume decrease in HL-60 cells

1994 ◽  
Vol 267 (4) ◽  
pp. C1057-C1066 ◽  
Author(s):  
K. R. Hallows ◽  
D. Restrepo ◽  
P. A. Knauf
Keyword(s):  
Intracellular Ph ◽  
Ph Regulation ◽  
Regulatory Volume Decrease ◽  
Transport Systems ◽  
Disulfonic Acid ◽  
Volume Dependence ◽  
Supportive Role ◽  
22Na Uptake ◽  
Volume Decrease ◽  
Stimulation Of

Intracellular pH (pHi) homeostasis was investigated in human promyelocytic leukemic HL-60 cells as they undergo regulatory volume decrease (RVD) in hypotonic media to determine how well pHi is regulated and which transport systems are involved. Cells suspended in hypotonic (50-60% of isotonic) media undergo a small (< 0.2 pH units), but significant (P < 0.05), intracellular acidification within 5 min. However, after 30 min of RVD, pHi is not significantly different from the initial pHi in 20 mM HCO3- medium and is significantly higher in HCO3(-)-free medium. Experiments performed in media with or without 150 microM 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid and HCO3- demonstrate that the anion exchanger (AE) mediates a net Cl- influx, with compensating HCO3- efflux, during RVD. To determine which transport systems are involved in counteracting this tendency toward acidification, we measured transport rates and examined the effect of transport system inhibitors on pHi. We found that inhibition of Na+/H+ exchange (NHE) with 12.5 microM ethylisoproplamiloride (EIPA) causes pHi to fall significantly by the end of 30 min of RVD. As assessed by EIPA-sensitive 22Na+ uptake measurements, NHE, largely dormant under resting isotonic conditions, becomes significantly activated by the end of 30 min of RVD, despite recovery of pHi and cell volume to near-normal levels. Thus a shift in the normal pHi dependence and/or volume dependence of NHE activity must occur during RVD under hypotonic conditions. In contrast, H(+)-monocarboxylate cotransport appears to play only a supportive role in pH regulation during RVD, as indicated by lack of stimulation of [14C]lactate efflux during RVD.

Na(+)-H+ antiporter and Na(+)-(HCO3-)n symporter regulate intracellular pH in mouse medullary thick limbs of Henle

1990 ◽  
Vol 258 (3) ◽  
pp. F445-F456 ◽  
Author(s):  
D. Kikeri ◽  
S. Azar ◽  
A. Sun ◽  
M. L. Zeidel ◽  
S. C. Hebert
Keyword(s):  
Steady State ◽  
Intracellular Ph ◽  
Dominant Role ◽  
Disulfonic Acid ◽  
Outer Medulla ◽  
Ethanesulfonic Acid ◽  
Antibody Labeling ◽  
Intracellular Alkalinization ◽  
Phi Regulation

To determine mechanisms of intracellular pH (pHi) regulation in mouse medullary thick limbs (MTAL), pHi was measured in MTAL suspensions and in the isolated perfused MTAL by use of 2',7'-bis(carboxyethyl)-5(6)carboxyfluorescein (BCECF). A method to obtain MTAL suspensions from the mouse outer medulla is reported. Characterization of suspensions with microscopy, anti-Tamm-Horsfall antibody labeling, measurement of O2 consumption, and adenosine 3',5'-cyclic monophosphate responses to antidiuretic hormone indicated that these suspensions were highly purified for viable MTAL tubules. The resting pHi was 7.41 +/- 0.02 (means +/- SE) in N-2-hydroxyethylpiperazine-N'-2-ethanesulfonic acid-buffered media and 7.23 +/- 0.02 in CO2- HCO3(-)-buffered media, both at extracellular pH 7.4. MTAL tubules exhibited rapid pHi recovery from intracellular acidification. Recovery of pHi was dependent on luminal Na+ (apparent Km = 13.2 +/- 3.2 mM) and was inhibited by amiloride (apparent Ki = 10.6 microM), consistent with the activity of an apical Na(+)-H+ antiporter. Antiporter activity was enhanced by acidification and was diminished at the resting pHi. Recovery from intracellular alkalinization (rapid withdrawal of CO2- HCO3-) was sensitive to the stilbene anion transport inhibitor 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid, Cl(-)-insensitive, and Na(+)-sensitive, consistent with the activity of a Na(+)-(HCO3-)n symporter. Both transporters were significantly involved in steady-state pHi regulation in the presence of CO2- HCO3-. In contrast, the Na(+)-H+ antiporter played the dominant role in steady-state pHi regulation in the absence of CO2- HCO3-.

Intracellular pH in snake renal proximal tubules

1995 ◽  
Vol 269 (4) ◽  
pp. R822-R829 ◽  
Author(s):  
Y. K. Kim ◽  
W. H. Dantzler
Keyword(s):  
Intracellular Ph ◽  
Basolateral Membrane ◽  
Distal Portion ◽  
Proximal Tubules ◽  
Disulfonic Acid ◽  
Renal Tubules ◽  
Garter Snakes ◽  
Luminal Membrane ◽  
Rate Of Recovery ◽  
Ethanesulfonic Acid

Intracellular pH (pHi) was studied in isolated proximal renal tubules of garter snakes (Thamnophis spp.) with oil-filled lumens under control conditions [N-2-hydroxyethylpiperazine-N'-2-ethanesulfonic acid (HEPES)-buffered medium with pH 7.4 at 25 degrees C] and in response to NH4Cl pulse. pHi was measured with the pH-sensitive fluorescent dye 2',7'-bis(2-carboxyethyl)-5,6-carboxyfluorescein (BCECF). Control resting pHi (7.1) and acidification in response to NH4Cl pulse (minimum pHi, 6.6) were essentially the same in snake tubules with oil-filled lumens or perfused lumens and in rabbit S2 proximal tubules with oil-filled lumens. Rate of recovery of pHi (dpHi/dt) from acid to resting level in snake tubules (2.5 x 10(-3) pH U/s was about one-third of that in rabbit tubules. Resting pHi and dpHi/dt from acid to resting level were Na+ dependent in the distal portion but not the proximal portion of snake proximal tubules. However, dpHi/dt was not influenced by amiloride or 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid in snake proximal tubules, suggesting that the effect of Na+ on dpHi/dt and resting pHi may involve membrane potential. This study also indicates that oil-filled lumens do not interfere with measurements of resting pHi and do permit evaluation of pHi regulation at the basolateral membrane without complications from transport at the luminal membrane.

Recovery from NMDA-induced intracellular acidification is delayed and dependent on extracellular bicarbonate

1996 ◽  
Vol 270 (2) ◽  
pp. C593-C599 ◽  
Author(s):  
L. M. Canzoniero ◽  
S. L. Sensi ◽  
D. W. Choi
Keyword(s):  
Intracellular Ph ◽  
Cortical Neurons ◽  
Nmda Antagonist ◽  
Disulfonic Acid ◽  
Intracellular Acidification ◽  
Subsequent Recovery ◽  
Cultured Cortical Neurons ◽  
Acidification Recovery ◽  
Dose Dependent ◽  
Stimulation Of

A 30-s exposure to N-methyl-D-aspartate (NMDA) produced a dose-dependent and long-lasting (10-20 min) reduction in intracellular pH in cultured cortical neurons, detected by the fluorescent dye 2',7'-bis(carboxyethyl)-5(6)-carboxyfluorescein. This intracellular acidification could be blocked by addition of the NMDA antagonist, D-(-)-2-amino-5-phosphonovalerate, or by removal of extracellular Ca2+. Removal of extracellular HCO3- markedly impaired recovery from NMDA-induced intracellular acidification. Recovery was also impaired when 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid or 4-acetamido-4'-isothiocyanostilbene-2,2'-disulfonic acid, inhibitors of HCO3- transport, were added to the cultures immediately after NMDA exposure. In contrast, the Na+/H+ exchange blocker, 5-(N-ethyl-N-isopropyl)amiloride, did not affect pH recovery. Removal of extracellular Cl- partially prevented pH recovery after NMDA stimulation. In addition, extracellular HCO3- increased intracellular Na+ after NMDA exposure, consistent with HCO3- activation of a Na(+)-dependent exchanger. These results demonstrate that stimulation of cortical neuronal NMDA receptors is followed by long-lasting intracellular acidification and that the presence of extracellular HCO3- is important in the subsequent recovery of normal intracellular pH, likely acting at least in part via the Na(+)-dependent Cl-/HCO3- exchanger.

Na(+)-HCO3- symport modulates intracellular pH in alveolar epithelial cells

1991 ◽  
Vol 260 (6) ◽  
pp. L555-L561 ◽  
Author(s):  
R. L. Lubman ◽  
E. D. Crandall
Keyword(s):  
Intracellular Ph ◽  
Initial Rate ◽  
Alveolar Epithelium ◽  
Alveolar Epithelial Cells ◽  
Transepithelial Transport ◽  
Disulfonic Acid ◽  
Experimental Conditions ◽  
Alveolar Epithelial ◽  
Ethanesulfonic Acid ◽  
Acid Extrusion

We investigated Na(+)-HCO3- cotransport as a mechanism for regulation of intracellular pH (pHi) in rat alveolar pneumocytes grown in primary culture. pHi was monitored using the fluorescent pH-sensitive dye 2',7'-bis(2-carboxyethyl)-5(6)-carboxyfluorescein (BCECF). Cells incubated in 6 mM N-2-hydroxyethylpiperazine-N'-2-ethanesulfonic acid (HEPES) medium at pH 7.4 were subjected to rapid acidification by CO2 pulse. pHi recovered in the presence of Na+ with an initial rate (dpHi/dt) of 0.15 min-1, which was reduced by 67% when Na+ was replaced by choline, unaffected by substitution of gluconate for Cl-, reduced 40% in the presence of 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid (DIDS, 500 microM), and unchanged by amiloride (1 mM). In parallel experiments, cells were incubated at pH 7.4 with 20 mM HCO3- and pHi acutely lowered by NH3 prepulse. dpHi/dt in these experiments was 0.14 min-1 in the presence of Na+ and HCO3-, and reduced 79% under Na(+)-free conditions. These data indicate the presence of a Na(+)-dependent, Cl(-)-independent, DIDS-sensitive and amiloride-insensitive mechanism of recovery from acute intracellular acidification in alveolar pneumocytes, most consistent with Na(+)-HCO3- cotransport (symport) effecting acid extrusion under these experimental conditions. This ion transport mechanism may contribute to regulation of pHi in alveolar pneumocytes, transepithelial transport of acid-base equivalents across the alveolar epithelium, and modulation of pH of alveolar fluid in adult mammalian lungs.

Proximal duodenal enterocyte transport: evidence for Na(+)-H+ and Cl(-)-HCO3- exchange and NaHCO3 cotransport

1993 ◽  
Vol 265 (4) ◽  
pp. G677-G685 ◽  
Author(s):  
J. I. Isenberg ◽  
M. Ljungstrom ◽  
B. Safsten ◽  
G. Flemstrom
Keyword(s):  
Intracellular Ph ◽  
Collagen Matrix ◽  
Ph Sensitive ◽  
Transport Processes ◽  
High Rate ◽  
Disulfonic Acid ◽  
Acid Base ◽  
Acetoxymethyl Ester ◽  
Addition And Subtraction ◽  
Ethanesulfonic Acid

The duodenum, in contrast to the jejunum, actively secretes HCO3- at a high rate, a process that protects the mucosa from acid/peptic injury. Our purpose was to define the mechanisms involved in HCO3- transport by studying the acid-base transport processes in isolated duodenal enterocytes. Individual rat duodenocytes, isolated by a combination of Ca2+ chelation and collagenase, attached to a collagen matrix were loaded with the pH-sensitive fluoroprobe 2',7'-bis(2-carboxyethyl)-5(6)-carboxyfluorescein acetoxymethyl ester (BCECF-AM), and intracellular pH was monitored by microfluorospectrophotometry. To identify Na(+)-H+ transport, cells in N-2-hydroxyethylpiperazine-N'-2-ethanesulfonic acid 1) were pulsed with NH4Cl (40 mM) in the absence and presence of amiloride and 2) were removed of Na+. To examine Cl(-)-HCO3- exchange, Cl- was removed from Ringer-HCO3- superfusate in the presence and absence of dihydro-4,4'-diisothiocyanostilbene-2,2'-disulfonic acid (H2DIDS). The NaHCO3 cotransporter was studied by addition and subtraction of Na+ to amiloride-treated and Cl(-)-depleted enterocytes perfused with Na(+)- and Cl(-)-free Ringer-HCO3- buffer with and without H2DIDS. Mammalian duodenocytes contain at least three acid-base transporters: an amiloride-sensitive Na(+)-H+ exchanger that extrudes acid, a DIDS-sensitive Cl(-)-HCO3- exchanger that extrudes base, and a NaHCO3 cotransporter, also DIDS sensitive, that functions as a base loader. These acid-base transporters likely play a key role in duodenal mucosal HCO3- secretion.(ABSTRACT TRUNCATED AT 250 WORDS)

Intracellular pH regulation in IEC-6 cells, a cryptlike intestinal cell line

1989 ◽  
Vol 257 (5) ◽  
pp. G732-G740 ◽  
Author(s):  
E. Wenzl ◽  
M. D. Sjaastad ◽  
W. H. Weintraub ◽  
T. E. Machen
Keyword(s):  
Cell Line ◽  
Intracellular Ph ◽  
Ph Regulation ◽  
Control Level ◽  
Intestinal Cell ◽  
Disulfonic Acid ◽  
Intestinal Crypt ◽  
Intestinal Cell Line ◽  
Ethanesulfonic Acid ◽  
Intestinal Crypt Cell

Regulation of intracellular pH, pHi, was studied using microspectrofluorimetry of the pH-sensitive, fluorescent dye 2',7'-bis(carboxyethyl)-5(6)-carboxyfluorescein in the rat intestinal crypt cell line, IEC-6. In N-2-hydroxyethylpiperazine-N'-2-ethanesulfonic acid (HEPES)-buffered solutions with pHi 7.25, treatment with a pulse of NH4Cl caused cells to acidify and then recover to control level. Because recovery was Na dependent, blocked by 1 mM amiloride, and unaffected by the presence and absence of Cl, it was likely because of a Na+-H+ exchanger. Cells were also acid loaded by changing from HEPES to HCO3-CO2-buffered solutions. pHi again recovered, but 1 mM amiloride reduced the rate of H+ efflux by only 47%. This HCO3-dependent, amiloride-insensitive H efflux required Na+ but not Cl- and was completely blocked by 200 microM [H2] 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid (DIDS). We conclude that a Na+-HCO3- cotransporter was operative. Cl-free solutions caused pHi to increase from 7.19 to 7.41; this effect required the presence of exogenous HCO3-CO2 but not Na and was blocked by 200 microM [H2]DIDS. A Cl- -HCO3- exchanger is the most likely explanation for these data. All the pHi regulatory mechanisms are operative in NaCl-HCO3-CO2-buffered solutions. The Na+-H+ and Na+-HCO3- mechanisms are acid extruders, whereas the Cl- -HCO3- exchanger is an acid loader. These transporters may be important for generating HCO3 secretion by intestinal crypt cells.

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