Influence of the external K+-concentration on the electrical activity and the Na+-, K+-content of the retinal tissue

1973 ◽  
Vol 341 (4) ◽  
pp. 297-304 ◽  
Author(s):  
U. Borchard ◽  
W. Erasmi
1987 ◽  
Vol 65 (5) ◽  
pp. 861-866 ◽  
Author(s):  
Normand Leblanc ◽  
Elena Ruiz-Ceretti ◽  
Denis Chartier

The influence of external potassium Ko and tetraethylammonium on the cellular K content of hypoxic myocardium was investigated. Perfused rabbit hearts were submitted to 60 min hypoxia in medium containing 5 mM K throughout or either low (1.5 mM) or high (10 mM) K during the last 20 min of hypoxia. Paced electrical activity (2.5 Hz) was kept throughout the experiments. Tissue samples excised from the left ventricle were analyzed for total water, inulin space, and Na and K content. Lowering Ko to 1.5 mM increased both K loss and Na accumulation. Addition of 3.5 mM RbCl under these conditions reversed Na accumulation to levels found for hypoxia in normal medium but did not modify the cellular K loss. Tetraethylammonium (10 mM) did not alter Na accumulation but partly prevented the decrease in K content produced by hypoxia. A similar effect was observed by increasing Ko to 10 mM. At this high Ko prolongation of hypoxia did not enhance K loss. Abolition of electrical activity by TTX in a high K solution prevented K loss and reduced the sodium content. These results are consistent with the view that voltage-dependent channels are implicated in the K loss induced by hypoxia or ischemia. Furthermore, they indicate that the K loss may be modulated by external K because of the influence of the electrochemical gradient on passive K efflux and thus provide an explanation for the existence of a plateau in the early extracellular K accumulation observed during cardiac ischemia.


1967 ◽  
Vol 50 (6) ◽  
pp. 1607-1625 ◽  
Author(s):  
J. A. Raven

The concentrations of K, Na, and Cl in the cytoplasm and vacuole, the tracer fluxes of these ions into and out of the cenocyte, and the electrical potential difference between bathing solution and vacuole and cytoplasm, have been measured in Hydrodictyon africanum. If the ions were acted on solely by passive electrochemical forces, a net efflux of K and Cl and a net influx of Na would be expected. Tracer fluxes indicate a net influx of K and Cl and efflux of Na in the light; these net fluxes are consequently active, with an obligate link to metabolism. The effects of darkness and low temperature indicate that most of the tracer K and Cl influx and Na efflux are linked to metabolism, while the corresponding tracer fluxes in the direction of the free energy gradient are not. Ouabain specifically inhibits the metabolically linked portions of tracer K influx and Na efflux. Alterations in the external K concentration have similar effects on metabolically mediated K influx and Na efflux. It would appear that K influx and Na efflux are linked, at least in the light.


1977 ◽  
Vol 232 (3) ◽  
pp. E294
Author(s):  
N Takeguchi ◽  
I Horikoshi ◽  
M Hattori

The K+ content in frog gastric mucosa (K+) was measured as a function of the submucosal K+ concentration ([K+sm]) in the absence of K+ on the mucosal side. The (K+) in HCO3- buffer with 95% O2-5% CO2 gas showed that the removal of external K+ induced a 27% K+ loss from the control value of 5 mM K+sm, that there was no linear relation between (K+) and [K+sm, and that the change in the (K+) versus the [K+sm] was hyperbolic, indicating that there are two different types of K+ in the mucosa: bound and free K+.


1989 ◽  
Vol 256 (6) ◽  
pp. C1214-C1223 ◽  
Author(s):  
D. M. Kaji

The kinetic properties of volume-sensitive K fluxes in swollen human erythrocytes were investigated. Swelling-activated Cl-dependent K influx was a saturable function of external K concentration with a low affinity (apparent Km of 115-130 mM) and high capacity [maximal velocity (Vmax) = 20-30 mmol.l original cells-1.h-1 (mmol.loc-1.h-1)]. The Vmax and apparent Km for Cl-dependent K efflux were lower (Km = 47 mM; Vmax = 2.2 mmol.loc-1.h-1). The Hill coefficients for both K efflux and influx were close to unity, suggesting a single binding site for K. The increase of external K trans-stimulated K efflux, but the increase of intracellular K had no effect on Cl-dependent K influx in swollen cells. Under zero trans conditions, the Vmax (18 vs. 3 mmol.loc-1.h-1) and Km (138 vs. 32) were markedly different for influx and efflux, respectively. These results provide evidence for intrinsic functional asymmetry, such that the transporter is more prevalent and stable in the outward-facing conformation. The mean ratio of Km to Vmax for efflux (12.1) was 1.56 times larger than the same ratio for influx (7.8), but the difference between the means did not reach statistical significance. These kinetic observations are analyzed in terms of the simple carrier and the cotransport models.


1994 ◽  
Vol 267 (5) ◽  
pp. E781-E788 ◽  
Author(s):  
K. A. Gregerson ◽  
N. Golesorkhi ◽  
R. Chuknyiska

Hypothalamic dopamine (DA) tonically inhibits prolactin (PRL) release from the anterior pituitary gland, whereas removal of DA markedly augments its release to values exceeding pre-DA rates. We investigated whether electrical events induced by DA contribute to this secretory rebound. In primary cultured lactotropes, spontaneous Ca(2+)-dependent spiking activity was enhanced after recovery from DA-induced hyperpolarization. Voltage clamp studies showed a rapidly and a slowly inactivating Ca2+ current that were both augmented by a hyperpolarizing conditioning potential. We measured PRL release from perifused cells exposed to DA to correlate the electrical with the secretory responses. DA inhibited PRL release by 67%, whereas PRL secretion increased three- to fourfold over basal release after washout of DA. Valinomycin, used to directly hyperpolarize the cell membrane, mimicked the actions of DA, inhibiting PRL release (65%) and, upon washout, augmenting PRL secretion. Blocking the DA- or valinomycin-induced hyperpolarization by elevating external K+ concentration blocked both the inhibition and rebound of PRL release. These novel results demonstrate that hyperpolarization of the lactotrope membrane by DA is critical for the development of PRL rebound after DA withdrawal. We hypothesize the mechanism involves the removal of inactivation from a population of Ca2+ channels, leading to enhanced Ca2+ influx and PRL release upon recovery of the resting membrane potential after DA removal.


1987 ◽  
Vol 65 (2) ◽  
pp. 246-251 ◽  
Author(s):  
Normand Leblanc ◽  
Elena Ruiz-Ceretti

The diffusion and electrogenic components of the resting potential of hypoxic ventricular muscle were separated by inhibition of the sodium pump with 10−4 M ouabain. The response to varying external K concentrations (Ko) was studied. Arteriaily perfused rabbit hearts were submitted to 60 min hypoxia in Krebs solution containing 5 mM K throughout or to different external K concentrations during the last 20 min of hypoxia. For K concentrations between 1.5 and 10 mM, hypoxia did not change the resting potential except for a slight hyperpolarization in 7.5 mM K. The diffusion component of the resting potential did not differ from the resting potential at Ko < 5 mM. An electrogenic potential of −3 to −6 mV was detectable at Ko values between 5 and 10 mM. The internal K concentration, Ki, was estimated from extrapolations to zero potential of the relation resting potential vs. Ko in normoxic and hypoxic hearts. These experiments revealed a decline of Ki of 16 mM with hypoxia. The variation of the diffusion potential with external K was fitted by a PNa:PK ratio five times lower than in normoxia. It has been concluded that an increase in K permeability and the persistence of electrogenic Na extrusion during hypoxia of rather short duration prevent membrane depolarization despite the myocardial K loss.


1962 ◽  
Vol 46 (2) ◽  
pp. 189-199 ◽  
Author(s):  
Ernest Page

The steady state transmembrane resting potential difference (Vm) has been measured in quiescent papillary muscles. Vm was determined as a function of the external K concentration in Cl and SO4 solutions and compared with the K equilibrium potential. Other measurements were made after replacement of external Na by choline, K by Rb and Cs, and Cl by SO4, CH3SO4, and NO3. Effects on Vm of albumin, temperature, and variation in internal K concentration are described.


1971 ◽  
Vol 58 (4) ◽  
pp. 413-437 ◽  
Author(s):  
Clay M. Armstrong

A number of compounds related to TEA+ (tetraethylammoniumion) were injected into squid axons and their effects on gK (the potassium conductance) were determined. In most of these ions a quaternary nitrogen is surrounded by three ethyl groups and a fourth group that is very hydrophobic. Several of the ions cause inactivation of gK, a type of ionic gating that is not normally seen in squid axon; i.e., after depolarization gK increases and then spontaneously decreases to a small fraction of its peak value even though the depolarization is maintained. Observations on the mechanism of this gating show that (a) QA (quaternary ammonium) ions only enter K+ channels that have open activation gates (the normal permeability gates). (b) The activation gates of QA-occluded channels do not close readily. (c) Hyperpolarization helps to clear QA ions from the channels. (d) Raising the external K+ concentration also helps to clear QA ions from the channels. Observations (c) and (d) strongly suggest that K+ ions traverse the membrane by way of pores, and they cannot be explained by the usual type of carrier model. The data suggest that a K+ pore has two distinct parts: a wide inner mouth that can accept a hydrated K+ ion or a TEA+-like ion, and a narrower portion that can accept a dehydrated or partially dehydrated K+ ion, but not TEA+.


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