Comments on: Sodium fluxes through the active transport pathway in toad bladder

1975 ◽  
Vol 24 (1) ◽  
pp. 401-406 ◽  
Author(s):  
A. Essig ◽  
M. A. Lang ◽  
M. Walser ◽  
J. S. Chen

1975 ◽  
Vol 21 (1) ◽  
pp. 87-98 ◽  
Author(s):  
Jing S. Chen ◽  
Mackenzie Walser


1982 ◽  
Vol 242 (3) ◽  
pp. R380-R389 ◽  
Author(s):  
J. K. Foskett ◽  
T. E. Machen ◽  
H. A. Bern

Effects of prolactin on transport properties of opercular membranes from seawater-adapted tilapia, Sarotherodon mossambicus, have been examined. These membranes are high conductance (average Gt approximately 4 mS.cm-2) tissues with short-circuit currents (I) equal to net chloride secretion. Despite high Gt, nonlinear current-voltage relationships suggest that opercular membranes cannot be classified as "leaky" tissues. Variability among membranes is reflected in a linear relationship between I and Gt with a slope equal to 26 mV and the zero-current Gt intercept equal to 0.45 mS.cm-2. Prolactin injections decrease I and Gt in a dose-dependent manner. Phosphodiesterase inhibition, without effect on I in untreated fish, often partially reverses these prolactin effects. Gt-I data from prolactin-treated fish yield a slope of 18 mV and a Gt intercept of 0.10 mS.cm-2. The effects of prolactin are discussed in terms of conventional equivalent circuit analysis. Discrepancies between predictions based on this model and the actual data indicate that an alternative interpretation, based on a heterogeneous cell population, is more accurate. Analysis of this circuit suggests that the ratio of paracellular to active transport pathway conductances associated with chloride cells is constant and that differences in Gt and I are due to parallel changes in these conductances. Prolactin may effectively "remove" chloride cells from these membranes as well as inhibit (reversible by elevated cellular cAMP levels) active transport pathway conductance of remaining cells.



1963 ◽  
Vol 205 (4) ◽  
pp. 718-722 ◽  
Author(s):  
Howard S. Frazier ◽  
Earle I. Hammer

A method of simultaneously determining the rates of loss of Na24 across the mucosal and serosal surfaces of the isolated toad bladder is described. The addition of vasopressin to the serosal medium causes an abrupt increase in the efflux of Na24 across the mucosal boundary, with no significant change in the efflux across the serosal surface. Replacement of sodium in the mucosal medium with choline causes no change in the efflux of Na24 across either the mucosal or serosal surfaces. The results indicate that the stimulation of active transport of sodium across the bladder after vasopressin is the result solely of an increase in the permeability to sodium of the mucosal surface. Vasopressin does not act directly on the active transport step at the serosal surface. In addition, the saturation kinetics which describe the process of sodium entry at the mucosal boundary are not the result of an exchange diffusion process, and appear not to be due to a sodium-induced change in the permeability of this surface to sodium.



Aldosterone, the major sodium retaining hormone in man, will stimulate active transport of sodium across the urinary bladder of the toad, Bufo marinus in vitro , at physiological concentrations of the hormone.The in vitro action of aldosterone is mimicked by steroid hormones with known mineralocorticoid properties and it is competitively inhibited by other analogues, e.g. spironolactone and cortisone. Aldosterone is bound to physiological receptor sites within the transporting epithelial cells, chiefly within the nuclei, and is displaced from these binding sites specifically by structural analogues including other mineralocorticoids. Effects of aldosterone are dependent upon availability of metabolizable substrates to support the active transport of sodium. Although the stimulation of sodium transport by aldosterone can be specifically inhibited by actinomycin D, an inhibitor of RNA synthesis, and by puromycin, an inhibitor of protein synthesis, direct evidence of stimulation of new RNA and protein synthesis during the latent period with physiological concentrations of aldosterone is still lacking. It is possible, however, that the amounts of RNA and protein that are involved are too small to be detected by available techniques. Evidence is summarized which leads us to conclude that the increased sodium transport induced by aldosterone is the consequence of a reduced resistance of the apical plasma membrane of the transporting epithelia to the entry of sodium into the transport pathway.



1984 ◽  
Vol 108 (1) ◽  
pp. 273-291
Author(s):  
M. V. THOMAS ◽  
T. E. MAY

Active potassium ion transport by isolated midguts of Spodoptera littoralis and Manduca sexta caterpillars has been studied by electrical means. In contrast to previous studies, the electrical properties of the midguts remained essentially constant for several hours; this improvement probably results from use of an experimental saline that more closely resembles caterpillar haemolymph. The active transport could be abolished by anoxia and by a number of chemical agents, of which trimethyl tin chloride (effective at 10−9M) was the most potent. Some of these substances, including trimethyl tin chloride, may have been acting directly on the potassium ion transport system. The results of varying the ionic composition of the saline suggest that potassium is the only cation that can be transported at a significant rate. However, the rate of potassium ion transport is increased by the simultaneous presence of other inorganic cations. Experiments to determine the ‘reversal potential’ for the active transport pathway, by varying the potassium ion concentration, suggested that this parameter was not a constant, and thus the active transport system could not be modelled by a simple equivalent electrical circuit, although the midgut epithelium is not unique in this respect. Therefore, the tissue electrical properties could not readily be correlated with the energetics of the potassium transport process, but the results are nevertheless consistent with a potassium ion: ATP ratio of greater than one, if ATP is indeed the primary energy source.





1976 ◽  
Vol 231 (4) ◽  
pp. 995-1001 ◽  
Author(s):  
TU Biber ◽  
TL Mullen

Measurement of Na efflux across the frog skin epithelium from the serosal side to the outside (JNa 3 leads to 1) in a new chamber specifically designed to avoid edge damage shows that JNa 3 leads to 1 exhibits saturation kinetics with a maximal efflux (Jmax) of 31.8 nmol/cm2 per h and an apparent KNa of 4.0 mM. In contrast, JNa 3 leads to 1 measured in conventional chambers and efflux determinations in the new chamber of substances that pass the epithelium via extracellular pathways (polyethylene glycol 900, sucrose, mannitol) exhibit a linear relationship between the efflux of the substance in question and its concentration in the bath. In addition, changes in external Na concentration do not cause substantial changes in JNa 3 leads to 1. The saturation remains but both Jmax and KNa increase after application of ouabain. Amiloride, as well as dinitrophenol, eliminates the saturation and JNa 3 leads to 1 becomes a linear function of Na concentration. The separate effects of ouabain and amiloride suggest that these two inhibitors which are known to affect two distinctly different steps in the active transport pathway act also on two separate steps of JNa 3 leads to 1: the passage across the inward- (serosal) and outward-facing (apical) cell membranes of the epithelial cells, respectively. The action of dinitrophenol indicates the involvement of metabolism in JNa 3 leads to 1 probably at the latter of the two steps. The results suggest strongly that JNa 3 leads to 1 proceeds not via a paracellular but via a transcellular pathway that interacts with the active transport pathway.





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