Intracellular potassium in cells of the distal tubule

Khuri, Raja N.; Agulian, S. K.; Kalloghlian, A.

doi:10.1007/bf00586220

Cited by 58 publications

(16 citation statements)

References 16 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…This possibility can be examined directly by comparing the differences in electrical potential and electrochemical potential for potassium across the basolateral plasma membranes of transporting ceils. Khuri and his collaborators have, in fact, reported results compatible with this concept in Necturus proximal tubule (Khuri et al, 1972b), and in rat proximal (Khuri, Agulian & Bogharian, 1974) and distal tubule (Khuri, Agulian and Kalloghlian, 1972a). On the other hand, potassium accumulation has been thought to exceed an electrochemical equilibrium distribution in frog skin (Jan~6ek, Morel & Bourguet, 1968), frog intestine (Lee & Armstrong, 1972), Chironomus salivary glands (Palmer & Civan, 1975), and urinary bladders of the toad Bufo bufojaponicus , and frog (Kimura & Fujimoto, 1977).…”

mentioning

confidence: 73%

Dissociation of cellular K+ accumulation from net Na+ transport by toad urinary bladder

DeLong

Civan

1978

J. Membrain Biol.

View full text Add to dashboard Cite

Summary.A number of published data suggest a variable stoichiometry between the rates of cellular potassium uptake and net sodium transport (JNa) across the urinary bladder of the toad. This problem was examined by simultaneously studying the iutracellular chemical activity of potassium (aK) with open-tip K+-selective microelectrodes and micropipets, and monitoring JNa by measuring the short-circuit current (SCC). When bathed in the short-circuited state with solutions containing an a• of 2.7 mrs, the mean + SEM values for intracellular aK were 43 _+ 0.6 m•.Ouabain, at a concentration of 10 -2 M, reduced intracellular aK by 56-67% and SCC by 96-100%. At 5 x 10 .4 M, ouabain reversibly reduced intracellular aK by 40-55%, and SCC by 63-68%; the inhibition of SCC was only partly reversible during the period of observation.Removal of external potassium reduced intracellular aK by 69-80% and SCC by 51-76%. Restoration of external potassium entirely returned intracellular aK to its control value, but only Partially reversed the inhibition of SCC during the period of study. Furthermore, recovery of aK began 19-43rain before that of SCC; recovery of aK was 90-97% complete before any increase in SCC could be measured. Although other interpretations are possible, the simplest interpretation of the data is that the processes responsible for potassium accumulation and transepithelial sodium transport are not identical. We propose the existence of a separate transfer mechanism at the basolateral cell membrane, responsible for accumulating intracellular potassium, and not directly coupled to active sodium transport.

show abstract

mentioning

confidence: 73%

Dissociation of cellular K+ accumulation from net Na+ transport by toad urinary bladder

DeLong

Civan

1978

J. Membrain Biol.

View full text Add to dashboard Cite

show abstract

“…In order to correlate the fluorescence excitation ratios with cell pH, the dye was calibrated intracellularly using the method of Thomas et [19]). …”

Section: Methodsmentioning

confidence: 99%

Basolateral membrane H/OH/HCO3 transport in the rat cortical thick ascending limb. Evidence for an electrogenic Na/HCO3 cotransporter in parallel with a Na/H antiporter.

Krapf

1988

J. Clin. Invest.

View full text Add to dashboard Cite

Mechanisms involved in basolateral H/OH/HCO3 transport in the in vitro microperfused rat cortical thick ascending limb were examined by the microfluorometric determination of cell pH using (2',7')-bis-(carboxyethyl)-(5,6)-carboxyfluorescein.The mean cell pH in this segment perfused with 147 mM sodium and 25 mM HCO3 at pH 7.4 was 7.13±0.02 (n = 30). Lowering bath HCO3 from 25 to 5 mM (constant Pco2 of 40 mmHg) acidified the cells by 0.31±0.02 pH units at a rate of 0.56±0.08 pH units/min. Removal of bath sodium acidified the cells by 0.28±0.03 pH units at a rate of 0.33±0.04 pH units/ min. The cell acidification was stilbene inhibitable and independent of chloride. There was no effect of bath sodium removal on cell pH in the absence of C02/HCO3. Depolarization of the basolateral membrane (step increase in bath potassium) independent of the presence of chloride. Cell acidification induced by bath sodium removal persisted when the basolateral membrane was voltage clamped by high potassium/valinomycin. Although these results are consistent with a Na/ (HCO3).>1 cotransporter, a Na/H antiporter was also suggested: 1 mM bath amiloride inhibited the cell pH defense against an acid load (rapid ammonia washout), both in the presence and absence of C02/HCO3, and inhibited the cell acidification induced by bath sodium reduction from 50 to 0 mM.In conclusion, an electrogenic Na/(HCO3),,,l cotransporter in parallel with a Na/H antiporter exist on the basolateral membrane of the rat cortical thick ascending limb.

show abstract

“…This is lower than the values of 163 and 142 mM obtained by Widdicombe, Basbaum and Highland (1981) and Cotton and Gatzy (1982) from chemical analysis of isolated tracheal cells, a difference of 25 to 33%. Discrepancies between cell K concentrations estimated using K-selective microelectrode techniques and chemical analysis have been reported for a variety of tissues including frog oocytes (Palmer, Century & Civan, 1978), Amphiuma small intestine (White, 1976), frog urinary bladder (Kimura & Fujimoto, 1977), toad urinary bladder (DeLong & Civan, 1980) and rat distal tubule (Khuri, Agulian & Kalloghlian, 1972). This probably represents compartmentation of cell K in organelles inaccessible to the electrode (Civan, 1980).…”

Section: Intracellular K Activitiesmentioning

confidence: 95%

Chloride secretion by canine tracheal epithelium: IV. Basolateral membrane K permeability parallels secretion rate

Smith

Frizzell

1984

J. Membrain Biol.

View full text Add to dashboard Cite

We evaluated the K conductance properties of the basolateral membranes of the surface cells of canine tracheal epithelium using microelectrode techniques. Studies were conducted under basal conditions (indomethacin, 10(-6) M, mucosal solution) and after stimulation of electrogenic Cl secretion with epinephrine (10(-6) M, serosal solution). Elevated serosal solution [K] depolarized the electrical potential differences across the apical (psi a) and basolateral (psi b) membranes in both the presence and absence of epinephrine. Serosal barium (0.5 mM) also depolarized psi a and psi b and selectively increased basolateral membrane resistance threefold. We also used K-selective microelectrodes to determine cell K activity (acK) and the driving force for K transport across the limiting membranes under basal and stimulated conditions. Stimulation of Cl secretion was not associated with significant changes in psi b or acK so that the driving force for K exit from cell to serosal solution (ca. 20 mV) was not altered. There was close agreement between the basolateral membrane electromotive force (Eb) determined from prior studies (M.J. Welsh, P.L. Smith and R.A. Frizzell, J. Membrane Biol. 71:209-218, 1983) and the chemical potential difference for K across this barrier (EbK) in the presence and absence of epinephrine. These findings support the notion that the basolateral membrane is characterized by a high conductance to K under both secreting and nonsecreting conditions and indicate that the decrease in basolateral membrane resistance that accompanies stimulation of Cl secretion results from an increase in its K conductance. This obviates changes in acK that would otherwise accompany increased Na/K pump activity and, by hyperpolarizing psi a, establishes the electrical driving force for Cl secretion across the apical membrane.

show abstract

Intracellular potassium in cells of the distal tubule

Cited by 58 publications

References 16 publications

Dissociation of cellular K+ accumulation from net Na+ transport by toad urinary bladder

Dissociation of cellular K+ accumulation from net Na+ transport by toad urinary bladder

Basolateral membrane H/OH/HCO3 transport in the rat cortical thick ascending limb. Evidence for an electrogenic Na/HCO3 cotransporter in parallel with a Na/H antiporter.

Chloride secretion by canine tracheal epithelium: IV. Basolateral membrane K permeability parallels secretion rate

Contact Info

Product

Resources

About