scholarly journals A small increment of external K concentration accelerates adrenomedullary catecholamine secretion induced by ouabain and metabolic inhibitors.

1983 ◽  
Vol 33 (4) ◽  
pp. 681-685 ◽  
Author(s):  
Masaru SORIMACHI ◽  
Shigeto NISHIMURA
1958 ◽  
Vol 193 (3) ◽  
pp. 534-538 ◽  
Author(s):  
Kenneth L. Zierler

Aldolase leak from rat peroneus longus muscle is assumed to occur by diffusion and its magnitude is taken to be an index of membrane permeability. Aldolase efflux is increased by high external K concentration, presumably owing to membrane depolarization. Mg lack may be slightly effective. Metabolic inhibitors, iodoacetate, dinitrophenol or cyanide, markedly increase aldolase efflux. These observations, with earlier ones on the effects of anoxia and of glucose lack, suggest that muscle membrane is labile, its permeability linked to cellular metabolism. A dynamic model of muscle membrane is proposed in which sites through which diffusion can occur ripple over the cell surface.


1996 ◽  
Vol 314 (2) ◽  
pp. 595-601 ◽  
Author(s):  
Fabienne DEFRISE-QUERTAIN ◽  
Chantal FRASER-L'HOSTIS ◽  
Danièle CORAL ◽  
Jacques DESHUSSES

The characteristics of the plasma-membrane potential of procyclic and bloodstream forms of Trypanosoma brucei brucei (cultured cells) were investigated using the fluorescent anionic probe bisoxonol. Observation of a stable and representative plasma-membrane potential in the resting state required careful washing, centrifugation and maintenance of the cells at room temperature before measurement. Bloodstream forms were more prone to depolarization during washing at 4 °C than procyclic cells. The higher fluorescence observed in the presence of long slender cells than in the presence of procyclic cells shows that the plasma-membrane potential is more negative in the insect form. Healthy dilute cells can sustain their plasma-membrane potential for hours in the presence of external glucose. The presence of a high K+ concentration in the medium did not promote by itself the depolarization of either type of cell. Study of bisoxonol fluorescence as a function of time allowed us to follow the kinetics of the action of metabolic inhibitors in the presence of various ions. o-Vanadate (1 mM) was found to depolarize bloodstream-form cells rapidly but only in a phosphate-free NaCl buffer. Omeprazole and strophanthidin also specifically depolarized bloodstream-form trypanosomes. However, NN´-dicyclohexylcarbodi-imide depolarized both types of cell, but more rapidly for bloodstream-form cells. Bloodstream-form trypanosomes appear to use mainly a vanadate-sensitive Na+ pump to maintain their Na+-diffusion gradient. However, most of the ATPase inhibitors tested had little or no effect on the plasma-membrane potential of procyclics suggesting that this form of trypanosome may rely on several regulation mechanisms.


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.


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