Regulation of K+ channels in the basolateral membrane ofNecturus oxyntic cells

Ueda, Shinichi; Loo, Donald D. F.; Sachs, George

doi:10.1007/bf01869612

Cited by 51 publications

(23 citation statements)

References 31 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…This increase in the peritubular K + conductance could account for most of the db-cAMP-induced hyperpolarization. It is now well-known that K+ conductance was increased by cAMP in other tissues (BENSON and LEVITAN, 1983;VEDA et al, 1987). Therefore, it would be reasonable to conclude that the hyperpolarization produced by db-cAMP was mainly due to the increase of K + conductance in the peritubular membrane of proximal tubule cell.…”

Section: Discussionmentioning

confidence: 94%

The effect of cAMP on ion transport in the proximal tubular cells in bullfrog kidney.

et al. 1988

View full text Add to dashboard Cite

Using a direct cellular micropuncture technique with doublebarreled ion-selective microelectrodes, we investigated the effect of dibutyryl-cyclic AMP (db-cAMP) on the membrane potential and the transport of Na +, K +, and H + in doubly-perfused bullfrog proximal tubules. The peritubular membrane potential difference (EM) and the intracellular K+, Na+ activities ((K);, (Na);) or intracellular and luminal pH were monitored continuously after peritubular administration of dbcAMP (10-3-10-4 M). Results: 1) db-cAMP hyperpolarized the EM by 8.0 mV with an increase of (K); by 4.8 mEq/l; 2) the peritubular administration of high K + (13.5 and 50 mM) solutions depolarized the EM by 11.5 and 41.5 mV, respectively. The high K + perfusate with db-cAMP produced a depolarization to the same level as that in simple high K + perfusion without db-cAMP; 3) db-cAMP transiently blocked the luminal acidification concomitantly with a cellular alkalinization by about 0.1 pH; and 4) db-cAMP caused a decrease of (Na); by 5.0 mEq/l. Conclusions: 1) cAMP causes an increase of K+ permeability in the peritubular membrane; 2) cAMP induces a cytosol alkalosis by enhancing incorporation of H+ into the subcellular vesicles, thus favoring the activation of Na+/K+ pump; and 3) cAMP, in effect, suppresses the Na+/H+ exchange mechanism in the luminal membrane and transiently blocks the proximal urinary acidification.

show abstract

Section: Discussionmentioning

confidence: 94%

The effect of cAMP on ion transport in the proximal tubular cells in bullfrog kidney.

et al. 1988

View full text Add to dashboard Cite

show abstract

“…Intracellular signaling events ultimately lead to the transition from the resting to the stimulated state. An H/ K-ATPase is activated in parallel with permeability pathways for both Cl and K on the apical canalicular face of the PC, whereas an anion exchanger provides pathways for Cl entry and HCO3 exit on the basolateral side of the cell (Ito and Schofield, 1974;Lee et al, 1979;Forte et al, 1981;Wolosin and Forte, 1984;Muallem et al, 1985Muallem et al, , 1988Paradiso et al, 1987; Ueda et al, 1987).…”

Section: Introductionmentioning

confidence: 99%

Regulation of Cl/HCO3 exchange in gastric parietal cells.

Thomas

Machen

1991

Cell Regul

View full text Add to dashboard Cite

Microspectrofluorimetry of the fluorescent indicators 2',7'-bis-(2-carboxyethyl)-5(and-6)carboxyfluorescein and 6-methoxy-N -(3-sulfopropyl) -quinolinium was used to measure intracellular pH (pHi), intracellular Cl (Cli), and transmembrane fluxes of HCO3 and Cl in single parietal cells (PC) in isolated rabbit gastric glands incubated in HCOJ C02-buffered solutions. Steady-state pHi was 7.2 in both resting (50 MM cimetidine) and stimulated (100 ,uM histamine) PCs. Transmembrane anion (HCO3 or Cl) flux rates during Cl removal from or readdition to the perfusate were the same in resting and stimulated PCs. These rates increased at alkaline pHi, though this pHi dependence was small in the physiological range. Maximum velocity (Vm,aJ for Cl influx or HCO3 effiux was 80-110 mM/min at pHi 7.6-7.8, and the Km for extracellular concentrations of Cl (Clo) was 25 mM; in the physiological range (pHi 7.1-7.3), V,,,. for anion fluxes was _50 mM/min. Steady-state Cli in the unstimulated PC was 62 ± 5 mM, but on histamine stimulation, Cli decreased rapidly to 25 mM and then increased back to a steady-state level of 44 mM. HCO3 fluxes due to Cl removal or readdition were completely blocked by 0.5 mM 4,4'-diisothiocyanatodihydrostilbene-2,2'-disulfonic acid (H2DIDS), but Cl fluxes were only inhibited by 80%. H2DIDS did not inhibit the decrease in Cli that occurred with histamine treatment. Diphenylamine carboxylate (0.5 mM) inhibited Cl flux by only 50% and caused no additional inhibition of Cl flux when used in conjunction with H2DIDS. Transmembrane anion fluxes during solution Cl removal or readdition occurred 80% through the anion exchanger at the basal membrane and 20% through other pathway(s), presumably the Cl channel in the apical membrane. We conclude that the increase in transport activity via the CI/HCO3 exchanger that occurs during histamine-induced increases in HCI secretion is due mostly to the decrease in Cli. In the resting cell with Cli = 62 mM, Clo = 120 mM, pHi = 7.2, and extracellular pH = 7.4, the anion exchanger is poised near its thermodynamic equilibrium. During histamine stimulation Cli drops from 62 mM to 44 mM, the thermodynamic equilibrium of the anion exchanger at the basolateral membrane is disturbed, and the anion exchanger then exchanges cellular HCO3 for extracellular Cl. Cli serves a crucial regulatory role in stimulus-secretion coupling in the PC.

show abstract

“…Although neither cell type is involved in transcellular Na transport, stimulation of these cells might be expected to affect Na turnover. For example, cell stimulation may activate a basolateral K conductance that should hyperpolarize the cell, thus aiding Cl secretion (Ueda et al, 1987) and resulting in a loss of cellular K. For the cell to maintain K under these conditions, entry of K via the Na/K pump needs to be stimulated, and this requires corresponding increases in Na influx, either directly or indirectly. Furthermore, there is evidence that stimulation of basolateral K channels in other Cl-secreting tissues causes concomitant stimulation of Na/K ATPase activity (Welsh et al, 1982;Smith and Frizzell, 1984).…”

Section: Introductionmentioning

confidence: 99%

Fluorescence measurements of cytosolic free Na concentration, influx and efflux in gastric cells.

et al. 1990

View full text Add to dashboard Cite

Regulation of cytosolic free Na (Na-) was measured in isolated rabbit gastric glands with the use of a recently developed fluorescent indicator for sodium, SBFI. Intracellular loading of the indicator was achieved by incubation with an acetoxymethyl ester of the dye. Digital imaging of fluorescence was used to monitor Na1 in both acid-secreting parietal cells and enzyme-secreting chief cells within intact glands. In situ calibration of Na; with ionophores indicated that SBFI fluorescence (345/385 nm excitation ratio) could resolve 2 mM changes in Nal and was relatively insensitive to changes in K or pH. Measurements on intact glands showed that basal Nal was 8.5 ± 2.2 mM in parietal cells and 9.2 ± 3 mM in chief cells. Estimates of Na influx and efflux were made by measuring rates of Na, change after inactivation or reactivation of the Na/K ATPase in a rapid perfusion system. Na/ K ATPase inhibition resulting from the removal of extracellular K (K) caused Na1 to increase at 3.2 ± 1.5 mM/min and 3.5 ± 2.7 mM/min in parietal and chief cells, respectively. Na buffering was found to be negligible. Addition of 5 mM K. and removal of extracellular Na (Na4) caused Na1 to decrease rapidly toward 0 mM Na. By subtracting passive Na efflux under these conditions (the rate at which Na1 decreased in Na-free solution containing ouabain), an activation curve (dNaJNaJ for the Na/K ATPase was calculated.The pump demonstrated the greatest sensitivity between 5 and 20 mM Nal. At 37°C the pump rate was <3 mM/min at 5 mM Na1 and 26 mM/min at 25 mM Nal, indicating that the pump has a great ability to respond to changes in Nal in this range. Carbachol, which stimulates secretion from both cell types, was found to stimulate Na influx in both cell types, but did not have detectable effects on Na efflux. dbcAMP+IBMX, potent stimulants of acid secretion, had no effect on Na metabolism.

show abstract

Regulation of K+ channels in the basolateral membrane ofNecturus oxyntic cells

Cited by 51 publications

References 31 publications

The effect of cAMP on ion transport in the proximal tubular cells in bullfrog kidney.

The effect of cAMP on ion transport in the proximal tubular cells in bullfrog kidney.

Regulation of Cl/HCO3 exchange in gastric parietal cells.

Fluorescence measurements of cytosolic free Na concentration, influx and efflux in gastric cells.

Contact Info

Product

Resources

About