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.

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)

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.

Membrane permeability during low potassium depolarization in sheep cardiac Purkinje fibers

1979 ◽  
Vol 237 (3) ◽  
pp. C156-C165 ◽  
Author(s):  
C. O. Lee ◽  
H. A. Fozzard
Keyword(s):  
Membrane Potential ◽  
Membrane Permeability ◽  
Resting Potential ◽  
Equilibrium Potential ◽  
Purkinje Fibers ◽  
Cardiac Purkinje Fibers ◽  
Low Potassium ◽  
Low K ◽  
Fiber Action ◽  
K Activity

Exposure of sheep Purkinje fibers to low [K]o leads to marked depolarization to a stable potential of about -40 mV. This level is equivalent to the plateau of the Purkinje fiber action potential. The low [K]o depolarization could be prevented by removal of [Na]o and was modified by tetrodotoxin. The membrane potential in the depolarized state was unresponsive to changes in [Cl]o or [Ca]o and it was poorly responsive to changes in [K]o between 0 and 2 mM. Repolarization was induced by decrease in [Na]o with a slope response of 30 mV/10-fold change in [Na]o. Average internal K activity (aK) in the resting state with a [K]o of 5 mM was 121.4 mM for a membrane potential of -80 mV. During low K depolarization aK was 119.7 mM with a membrane potential of -34 mV. The depolarization was therefore due to a change in membrane permeability, with little change in aK. Upon restoration of [K]o the fiber repolarized to values transiently more negative than the prior resting potential. These transient potentials were more negative than the K equilibrium potential (VK), if it is calculated assuming a uniform [K]o. The hyperpolarization was reduced by ouabain [10(-6)] or by low [Ca]o.

Effects of Ca2+/Mg2+ removal on aiNa, aiK, and tension in cardiac Purkinje fibers

1986 ◽  
Vol 251 (6) ◽  
pp. C920-C927 ◽  
Author(s):  
R. A. Chapman ◽  
H. A. Fozzard ◽  
I. R. Friedlander ◽  
C. T. January
Keyword(s):  
Divalent Cations ◽  
Calcium Paradox ◽  
Purkinje Fibers ◽  
Intracellular Na Activity ◽  
Cardiac Purkinje Fibers ◽  
Channel Blocking ◽  
Ionic Changes ◽  
Ion Sensitive Microelectrodes ◽  
Intracellular K Activity ◽  
K Activity

Sheep cardiac Purkinje fibers were exposed to solutions free of divalent cations for hour-long periods, while intracellular Na+ and K+ activities were measured using ion-sensitive microelectrodes. Intracellular Na+ activity (aiNa) increased to 50.1 +/- 8.1 mM, and intracellular K+ activity (aiK) decreased to 76.7 +/- 3.5 mM. These ionic changes could be blocked by the presence of Mg2+ or the Ca2+ channel blocking agents D 600 and nifedipine. The rise in aiNa and the fall in aiK was accentuated by the inhibition of the Na+-K+ pump with acetylstrophanthidin or by removal of extracellular K+. These results demonstrate that in cardiac Purkinje fibers removal of divalent cations produces intracellular loading of Na+ by Na+ entry through the Ca2+ channel. On reexposure to Ca2+-containing solutions, the cells become loaded with Ca2+, and the fibers exhibit large contractures. These observations implicate Na+-Ca2+ exchange in the entry of Ca2+ into these cells during Ca2+ repletion and in the etiology of the calcium paradox.

Role of calcium in caffeine-norepinephrine interactions in cardiac Purkinje fibers

1989 ◽  
Vol 257 (1) ◽  
pp. H226-H237 ◽  
Author(s):  
H. Satoh ◽  
M. Vassalle
Keyword(s):  
Calcium Concentration ◽  
Iodoacetic Acid ◽  
Slow Inward Current ◽  
Extracellular Potassium ◽  
Purkinje Fibers ◽  
Extracellular Potassium Concentration ◽  
Cardiac Purkinje Fibers ◽  
Ca Uptake

Caffeine-norepinephrine interactions were studied in canine cardiac Purkinje fibers perfused in vitro. Caffeine (0.5-1 mM) or theophylline (0.5-1 mM) increased and then decreased contractile force in the absence and presence of 0.5-10 microM norepinephrine (NE) [in high extracellular calcium concentration ([Ca]o) caffeine only decreases force]. Occasionally, caffeine only decreased force in the presence of NE. In the presence of NE and 12 mM (sometimes even 4 mM) extracellular potassium concentration, caffeine did not decrease force below the precaffeine level. Reciprocally, in 0.5-2 mM caffeine NE increased force, although less than in the absence of caffeine. Even in 9 mM caffeine, NE increased force but slowed the final phase three repolarization of the action potential. Both NE and 8.1 mM [Ca]o increased force, but NE decreased force in the presence of high [Ca]o. In NE and propranolol (or propranolol alone), caffeine only increased force, whereas it had the usual effects in the presence of methoxamine or phenotolamine. In the presence of iodoacetic acid and 2-deoxy-D-glucose, NE caused contracture and caffeine exaggerated it. In contrast, in NE and 2 mM Mn, caffeine only increased force. It is concluded that initially NE diminishes the cytoplasmic calcium overload induced by caffeine (by promoting Ca uptake into the sarcoplasmic reticulum) and subsequently enhances it (by increasing the slow inward current).

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.

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