Transepithelial transport and its hormonal control in toad bladder

Author(s):  
Alexander Leaf



1981 ◽  
Vol 77 (6) ◽  
pp. 693-712 ◽  
Author(s):  
H S Chase ◽  
Q Al-Awqati

Sodium movement across the luminal membrane of the toad bladder is the rate-limiting step for active transepithelial transport. Recent studies suggest that changes in intracellular sodium regulate the Na permeability of the luminal border, either directly or indirectly via increases in cell calcium induced by the high intracellular sodium. To test these proposals, we measured Na movement across the luminal membrane (th Na influx) and found that it is reduced when intracellular Na is increased by ouabain or by removal of external potassium. Removal of serosal sodium also reduced the influx, suggesting that the Na gradient across the serosal border rather than the cell Na concentration is the critical factor. Because in tissues such as muscle and nerve a steep transmembrane sodium gradient is necessary to maintain low cytosolic calcium, it is possible that a reduction in the sodium gradient in the toad bladder reduces luminal permeability by increasing the cell calcium activity. We found that the inhibition of the influx by ouabain or low serosal Na was prevented, in part, by removal of serosal calcium. To test for the existence of a sodium-calcium exchanger, we studied calcium transport in isolated basolateral membrane vesicles and found that calcium uptake was proportional to the outward directed sodium gradient. Uptake was not the result of a sodium diffusion potential. Calcium efflux from preloaded vesicles was accelerated by an inward directed sodium gradient. Preliminary kinetic analysis showed that the sodium gradient changes the Vmax but not the Km of calcium transport. These results suggest that the effect of intracellular sodium on the luminal sodium permeability is due to changes in intracellular calcium.



1994 ◽  
Vol 74 (2) ◽  
pp. 305-322 ◽  
Author(s):  
C. de Rouffignac ◽  
G. Quamme

Our understanding of renal Mg handling has been expanded in recent years with the use of electron probe, ultramicroanalysis, and fluorescent dye techniques to determine total Mg and free Mg2+ in individual tubule segments and cells, respectively. Recent studies have shown that [Mg2+]i is a highly mobile cation that may be altered by a number of influences including hormones. It is likely that the hormonal changes in [Mg2+]i, reported here and elsewhere, are involved in intracellular metabolism and regulation rather than transepithelial transport. The role of intracellular Mg2+ in control of cell function is poorly understood. However, it is evident that [Mg2+]i may be rapidly charged through a number of different influences that may have important effects on cell function. These kinds of data have enlarged our understanding of Mg conservation by the renal tubule but have posed many questions for further study. Magnesium is handled in different ways along the nephron. About 80% of the total plasma Mg (1.5-2.0 mM) is ultrafilterable across the glomerular membrane. Of the ultrafilterable Mg (1.2-1.6 mM), only 20-25% is reabsorbed by the proximal tubule, including the convoluted and straight portions. This is in contrast to Na and Ca reabsorption, which amounts to approximately 70 and 60%, respectively, in the proximal nephron. Accordingly, the fractional delivery of Mg to the thick ascending limb of the loop of Henle is much greater than that of Na or Ca. It is now evident from micropuncture studies that proportionally greater amounts of Mg (50-60%) are reabsorbed in the loop compared with Na (20-25%) or Ca (30-35%). Because the terminal nephron segments, including the DCT and collecting tubule, reabsorb only a small portion of the filtered Mg (approximately 5%), the loop of Henle plays a major role in the determination of Mg reabsorption, and it is in this segment that the major regulatory factors act to maintain Mg balance. Magnesium reabsorption in the thick ascending limb takes place in the cortical segments, at least in the mouse and rat. Evidence summarized here suggests that Mg is passively reabsorbed via the paracellular pathway in the cTAL of the loop of Henle. Several factors affect Mg reabsorption in the loop of Henle. Hypermagnesemia and hypercalcemia inhibit reabsorption leading to increased urinary excretion of Mg and Ca. These effects have been reviewed in detail elsewhere (113, 149). Magnesium depletion, for instance through dietary Mg deprivation, enhances Mg reabsorption in the loop of Henle before the fall in plasma Mg concentration and filtered Mg load.(ABSTRACT TRUNCATED AT 400 WORDS)





1977 ◽  
Vol 137 (4) ◽  
pp. 495-501 ◽  
Author(s):  
J. D. McGarry
Keyword(s):  


1958 ◽  
Vol 28 (2_Suppl) ◽  
pp. S41-S45
Author(s):  
G. A. Overbeek
Keyword(s):  


1973 ◽  
Vol 74 (1) ◽  
pp. 201-208 ◽  
Author(s):  
D. Maor ◽  
E. Eylan ◽  
P. Alexander

ABSTRACT Ribonuclease activity in thymus and lymph nodes is stimulated by cortisone; insulin increases ribonuclease activity only in the thymus. Growth hormone and theophylline do not cause changes in thymus and lymph nodes ribonuclease levels. Injections of cortisone combined with growth hormone or with theophylline increase the activity more than cortisone alone. Insulin does not enhance the action of cortisone on ribonuclease activity. A synergistic loss in weight of thymus and spleen was found after administration of cortisone in combination with either growth hormone or with theophylline.





2015 ◽  
Author(s):  
Shelley E Harris ◽  
Amy Kelly ◽  
Melissa A Davis ◽  
Miranda Anderson ◽  
Alison J Forhead ◽  
...  


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