Effects of anisosmotic medium on cell volume, transmembrane potential and intracellular K+ activity in mouse hepatocytes

1987 ◽  
Vol 100 (1) ◽  
pp. 53-61 ◽  
Author(s):  
Larry D. Howard ◽  
Robert Wondergem
Keyword(s):  
Cell Volume ◽  
Transmembrane Potential ◽  
Mouse Hepatocytes ◽  
Intracellular K Activity ◽  
K Activity

Association between HCO3(-) absorption and K+ uptake by Amphiuma jejunum: relations among HCO3(-) absorption, luminal K+, and intracellular K+ activity

1984 ◽  
Vol 246 (6) ◽  
pp. G732-G744
Author(s):  
M. A. Imon ◽  
J. F. White
Keyword(s):  
Short Circuit ◽  
Short Circuit Current ◽  
Uptake Mechanism ◽  
Bathing Medium ◽  
The Media ◽  
Absorptive Flux ◽  
Free Media ◽  
Intracellular K Activity ◽  
K Activity

Titration techniques and K+- sensitive microelectrodes have been used to investigate the relations among HCO3(-) absorption, luminal K+, and intracellular K+ activity in in vitro Amphiuma jejunum. The HCO3(-) absorptive flux (JHCO3(-] measured by pH-stat under short circuit was reduced by removal of K+ from the medium but not by replacement of Na+ with choline. JHCO3(-) exhibited a seasonal variation when K+ was absent from the media and was increased to a maximum when K+ equaled 5 mM. Addition of K+ to a K+-free luminal medium stimulated JHCO3(-) much more than addition to the serosal medium. Acetazolamide (10(-4) M) blocked K+-stimulated HCO3(-) absorption while benzolamide reduced the short-circuit current associated with HCO3(-) absorption much more rapidly when added to the mucosal bathing medium. Intracellular K+ activity (aik) and mucosal membrane potential (psi m) of jejunal villus cells were measured with double-barreled microelectrodes. When bathed bilaterally with HCO3(-)-containing media, K+ was actively accumulated for many hours (aik = 58.5 mM) but in the presence of ouabain fell to equilibrium (16 mM) after 2 h. In contrast, when HCO3(-) absorption was induced by removal of serosal HCO3(-), aik was elevated to 83.6 mM and, after 4-h exposure to ouabain cell K+, remained far above electrochemical equilibrium at 33 mM. Tissues bathed in Na+-free (Tris) media containing ouabain retained cell K+ after 4 h at even higher levels (46 mM). Cell K+ activity was reduced by removal of K+ from either the mucosal or serosal medium. Acetazolamide reduced aik over 2 h in Na+-free media from 66 to 42 mM. The decline in aik was associated with a concomitant decline in the HCO3(-) absorptive current. It is concluded that K+ is actively accumulated across both luminal and serosal membranes of the jejunal absorptive cell and that the luminal uptake mechanism is linked to HCO3(-) absorption or an equivalent process.

Basal membrane uptake in potassium-secreting cells of midgut of tobacco hornworm (Manduca sexta)

1990 ◽  
Vol 258 (1) ◽  
pp. R112-R119
Author(s):  
A. C. Chao ◽  
A. R. Koch ◽  
D. F. Moffett
Keyword(s):  
Manduca Sexta ◽  
Short Circuit ◽  
Short Circuit Current ◽  
Basal Membrane ◽  
Bathing Solution ◽  
K Uptake ◽  
Active Secretion ◽  
Uptake Process ◽  
Intracellular K Activity ◽  
K Activity

Basal membrane voltage (Vb), intracellular K+ activity [(K+)i], and short-circuit current (Isc) were measured in isolated posterior midguts of Manduca sexta wherein Isc is a measured of active secretion of K+ from blood into lumen. When bathed in 32 mM K+ and exposed to 100% O2, average values were Isc = 244 microAmp/cm2, Vb = -33.1 mV, and (K+)i = 88.6 mM. The electrochemical gradient across the basal membrane (d mu) averaged +5.8 mV (a gradient favorable for K+ entry). Exposure to 5% O2 led to a new steady state in which Isc = 71 microAmp/cm2, Vb = -18.7 mV, and (K+)i = 99.4 mM. During hypoxia, d mu averaged -9.9 mV (a gradient unfavorable for K+ entry). When the external bathing solution was 10 mM K+, comparable values were, for 100% O2, Isc = 139 microAmp/cm2, Vb = -56.1 mV, (K+)i = 72.2 mM, and d mu = +3.6 mV, and in 5% O2 the values were Isc = 28.3 microAmp/cm2, Vb = -43.7 mV, (K+)i = 76.1 mM, and d mu = -10.2 mV. The failure of cellular K+ to fall during prolonged hypoxia is evidence for a thermodynamically active basal K+ uptake process.

Potassium distribution and membrane potential of sensory neurons in the leech nervous system

1984 ◽  
Vol 51 (4) ◽  
pp. 689-704 ◽  
Author(s):  
W. R. Schlue ◽  
J. W. Deitmer
Keyword(s):  
Nervous System ◽  
Membrane Potential ◽  
Sensory Neurons ◽  
Membrane Resistance ◽  
Equilibrium Potential ◽  
Bathing Medium ◽  
Membrane Hyperpolarization ◽  
K Concentration ◽  
Intracellular K Activity ◽  
K Activity

The intracellular K activity (aKi) and membrane potential of sensory neurons in the leech central nervous system were measured in normal and altered external K+ concentrations, [K+]o, using double-barreled, liquid ion-exchanger microelectrodes. In control experiments membrane potential measurements were made using potassium chloride-filled single-barreled microelectrodes. All values are means +/- SD. At the normal [K+]o (4 mM) the mean aKi of all cells tested was 72.6 +/- 10.6 mM (n = 40) and the average membrane potential was -47.3 +/- 5.2 mM (n = 40). When measured with single-barreled microelectrodes, the membrane potential averaged -45.3 +/- 2.9 mV (n = 12). Assuming an intracellular K+ activity coefficient of 0.75, the intracellular K+ concentration of sensory neurons would be 96.8 +/- 14.1 mM). With an extracellular K+ concentration of 5.8 mM in the intact ganglion compared to the K+ concentration of 4 mM in the bath, the K+ equilibrium potential was -71.5 mV. When the ganglion capsule was opened, the extracellular K+ concentrations in the ganglion were similar to that of the bathing medium and the calculated K+ equilibrium potential was -81 mV. The membrane of sensory neurons depolarized following the changes to elevated [K+]o (greater than or equal to 10-100 mM), whereas aKi changed only little or not at all. At very low [K+]o (0.2, 0 mM) aKi and membrane potential showed little short-term (less than 3 min) effect but began to change after longer exposure (greater than 3 min). Reduction of [K+]o from 4 to 0.2 mM (or 0 mM) produced first a slow, and then a more rapid decrease of aKi and membrane resistance, accompanied by a slow membrane hyperpolarization. Following readdition of normal [K+]o, the membrane first depolarized and then transiently hyperpolarized, eventually returning slowly to the normal membrane potential.(ABSTRACT TRUNCATED AT 400 WORDS)

Change of intracellular K+ activity in rat soleus muscle during hypokalemia

1989 ◽  
Vol 22 (6) ◽  
pp. 1009-1013 ◽  
Author(s):  
Ryoji Nagaoka ◽  
Satoru Yamashita ◽  
Norio Akaike
Keyword(s):  
Soleus Muscle ◽  
Rat Soleus Muscle ◽  
Intracellular K Activity ◽  
K Activity

Microelectrode measurements of K+ and pH in rabbit gastric glands: effect of histamine

1984 ◽  
Vol 246 (4) ◽  
pp. G433-G444
Author(s):  
K. Kafoglis ◽  
S. J. Hersey ◽  
J. F. White
Keyword(s):  
Membrane Potential ◽  
Ion Exchange ◽  
Basolateral Membrane ◽  
Free Medium ◽  
Na Transport ◽  
K Uptake ◽  
Gastric Glands ◽  
Microelectrode Measurements ◽  
Intracellular K Activity ◽  
K Activity

Conventional and liquid ion-exchange microelectrodes sensitive to K+ or pH were used to examine the response of isolated rabbit gastric glands to histamine. The epithelial cells were impaled across the basolateral membrane. The membrane potential averaged -6.1 +/- 0.6 mV and was unchanged after replacement of medium K+, Cl-, or Na+. The intracellular K+ activity (alpha iK) averaged 41.3 +/- 3.0 mM, indicating K+ accumulation by a factor of 6.8. Active accumulation of K+ was eliminated by ouabain. In contrast, histamine increased K+ activity to 55.3 +/- 3.9 mM. This stimulation was blocked by ouabain. In glands bathed in a Na+-free medium containing ouabain, addition of histamine elevated alpha iK from 12.5 +/- 0.7 to 17.1 +/- 1.1 mM. Isobutylmethylxanthine (10(-4) M) also elevated alpha iK. When impaled with pH-sensitive microelectrodes, glands exposed to histamine exhibited regions of acidity as low as pH 3. Acidification was also produced by histamine after medium Na+ had been replaced with choline. Picoprazole (H 149/94) blocked the effects of histamine on alpha iK and gland pH. The results are consistent with the view that histamine-induced acid secretion by gastric glands is associated with K+ uptake by a mechanism that is independent of Na+ transport but is inhibited by intracellular Na+. This is most likely the H+-K+-ATPase on the secretory surface of the gland cells. Evidence that some tissue K+ is bound or compartmentalized is also discussed.

scholarly journals The effect of extracellular potassium on the intracellular potassium ion activity and transmembrane potentials of beating canine cardiac Purkinje fibers.

1977 ◽  
Vol 69 (4) ◽  
pp. 463-474 ◽  
Author(s):  
D S Miura ◽  
B F Hoffman ◽  
M R Rosen
Keyword(s):  
Equilibrium Potential ◽  
Extracellular Potassium ◽  
Purkinje Fibers ◽  
Transmembrane Potentials ◽  
Cardiac Purkinje Fibers ◽  
K Concentration ◽  
Range Of Values ◽  
Intracellular K Activity ◽  
Liquid Ion Exchanger ◽  
K Activity

We used open tip microelectrodes containing a K+-sensitive liquid ion exchanger to determine directly the intracellular K+ activity in beating canine cardiac Purkinje fibers. For preparations superfused with Tyrode's solution in which the K+ concentration was 4.0 mM, intracellular K+ activity (ak) was 130.0+/-2.3 mM (mean+/-SE) at 37 degrees C. The calculated K+ equilibrium potential (EK) was -100.6+/-0.5 mV. Maximum diastolic potential (ED) and resting transmembrane potential (EM) were measured with conventional microelectrodes filled with 3 M KCl and were -90.6+/-0.3 and -84.4+/-0.4 mV, respectively. When [K+]o was decreased to 2.0 mM or increased to 6.0, 10.0, and 16.0 mM, ak remained the same. At [K+]o=2.0, ED was -97.3+/-0.4 and Em -86.0+/-0.7 mV; at [K+]o=16.0, ED fell to -53.8+/-0.4 mV and Em to the same value. Over this range of values for [K+]o, EK changed from -119.0+/-0.3 to -63.6+/-0.2 mV. These values for EK are consistent with those previously estimated indirectly by other techniques.

Measurements of the Intracellular Potassium Activity of Retzius Cells in the Leech Central Nervous System

1981 ◽  
Vol 91 (1) ◽  
pp. 87-101
Author(s):  
JOACHIM W. DEITMER ◽  
WOLF R. SCHLUE
Keyword(s):  
Cell Membrane ◽  
External Solution ◽  
Equilibrium Potential ◽  
The Mean ◽  
K Concentration ◽  
Retzius Cells ◽  
Intracellular K Activity ◽  
K Permeability ◽  
K Activity ◽  
External K

The intracellular K activity of leech Retzius cells was measured using double-barrelled, liquid ion exchanger, microelectrodes. At the normal external K+ concentration of 4 mm (equivalent to 3 mm-K activity, assuming an activity coefficient of 0.75) the mean K activity was 101.3 ± 7.6 mm (S.D., n = 14) in the cell bodies, and 4.35 ± 0.4 mV (n = 27) in the extracellular spaces surrounding them, indicating a K+ equilibrium potential of - 80 mV. The mean membrane potential was - 43.6 + 4.9 mV (n = 14). In a K-free external solution, or in the presence of 5 × 10−4m-ouabain, the intracellular K activity decreased by up to 14 mm min−1. This indicates an efflux of K+ ions across the cell membrane of approximately 2 × 10−10 mol cm−2s, and an apparent K+ permeability coefficient of 8 × 10−8 cms−1. The cell membrane depolarized upon removal of K+ and upon addition of ouabain, and transiently hyperpolarized beyond its initial level on return to the normal external K+ concentration. The recovery from this hyperpolarization paralleled the increase of the intracellular K activity following the re-addition of K+. Our results suggest that, despite the high K+ permeability of the Retzius cell membrane, the intracellular K activity is maintained at a high level by an electrogenic pump.

scholarly journals Intracellular K+ activity and its relation to basolateral membrane ion transport in Necturus gallbladder epithelium.

1980 ◽  
Vol 76 (1) ◽  
pp. 33-52 ◽  
Author(s):  
L Reuss ◽  
S A Weinman ◽  
T P Grady
Keyword(s):  
Cell Membrane ◽  
Amphotericin B ◽  
Basolateral Membrane ◽  
Membrane Potentials ◽  
Equilibrium Potential ◽  
Gallbladder Epithelium ◽  
Bathing Medium ◽  
Necturus Gallbladder ◽  
Intracellular K Activity ◽  
K Activity

A study of the mechanisms of the effects of amphotericin B and ouabain on cell membrane and transepithelial potentials and intracellular K activity (alpha Ki) of Necturus gallbladder epithelium was undertaken with conventional and K-selective intracellular microelectrode techniques. Amphotericin B produced a mucosa-negative change of transepithelial potential (Vms) and depolarization of both apical and basolateral membranes. Rapid fall of alpha Ki was also observed, with the consequent reduction of the K equilibrium potential (EK) across both the apical and the basolateral membrane. It was also shown that, unless the mucosal bathing medium is rapidly exchanged, K accumulates in the unstirred fluid layers near the luminal membrane generating a paracellular K diffusion potential, which contributes to the Vms change. Exposure to ouabain resulted in a slow decrease of alpha Ki and slow depolarization of both cell membranes. Cell membrane potentials and alpha Ki could be partially restored by a brief (3-4 min) mucosal substitution of K for Na. Under all experimental conditions (control, amphotericin B, and ouabain), EK at the basolateral membrane was larger than the basolateral membrane equivalent emf (Eb). Therefore, the K chemical potential difference appears to account for Eb and the magnitude of the cell membrane potentials, without the need to postulate an electrogenic Na pump. Comparison of the rate of Na transport across the tissue with the electrodiffusional K flux across the basolateral membrane indicates that maintenance of a steady-state alpha Ki cannot be explained by a simple Na,K pump-K leak model. It is suggested that either a NaCl pump operates in parallel with the Na,K pump, or that a KCl downhill neutral extrusion mechanism exists in addition to the electrodiffusional K pathway.

Sign in / Sign up

Export Citation Format

Share Document