Mechanism of inhibition of the proximal tubular isotonic fluid absorption by polylysine and other cationic polyamino acids

1975 ◽  
Vol 21 (1) ◽  
pp. 311-334 ◽  
Author(s):  
Kenzo Sato ◽  
Karl J. Ullrich
1979 ◽  
Vol 236 (2) ◽  
pp. F89-F96 ◽  
Author(s):  
T. E. Andreoli ◽  
J. A. Schafer

This Editorial Review summarizes certain considerations relevant to the mechanism(s) of isotonic fluid absorption by the mammalian proximal nephron. Recent evidence indicates that the paracellular pathway in this epithelium has a low diffusion resistance. Therefore it is possible that lateral intercellular spaces are in diffusion equilibrium with the peritubular medium. For such a circumstance, the driving forces for isotonic fluid absorption may reside in external solutions. But since the hydraulic conductance of mammalian proximal tubules is remarkably high, the effective osmotic pressure gradient between luminal and pertibular solutions required to drive isotonic fluid transport is relatively small. In the mammalian proximal nephron, effective luminal hypotonicity may provide the driving force for isotonic fluid transport. At least two mechanisms could account for the development of effective luminal hypotonicity. First, preferential absorption of bicarbonate results in a rise of luminal Cl- concentration. And because proximal tubules are more permeable to Cl- than to HCO3-, there develops a driving force for isotonic fluid transport. Second, trivial degrees of luminal hypotonicity may develop attendant on active Na+ absorption. We provide evidence that, of these two mechanisms, axial anion asymmetry is the dominant force for isotonic fluid transport.


2004 ◽  
Vol 31 (5-6) ◽  
pp. 348-353 ◽  
Author(s):  
Valentina Jovanovska ◽  
Eveline Eitle ◽  
Peter J Harris

2005 ◽  
Vol 103 (1) ◽  
pp. 203-204 ◽  
Author(s):  
Monika Schäfer ◽  
Britta S. Von Ungern-Sternberg ◽  
Edward Wight ◽  
Markus C. Schneider

1981 ◽  
Vol 240 (6) ◽  
pp. F558-F568 ◽  
Author(s):  
P. A. Friedman ◽  
J. F. Figueiredo ◽  
T. Maack ◽  
E. E. Windhager

The effect of experimental maneuvers believed to raise cytosolic [Ca2+] on Na and fluid absorption by isolated perfused proximal convoluted tubules of rabbit kidneys was examined. For this purpose experiments were carried out in which either 1) peritubular [Na] was lowered from 145 mM in controls to 40 mM in experimental periods by isosmotic replacement with Li, tetraethylammonium, or choline; or 2) quinidine (10(-4) M) or A 23187 (5 X 10(-6) M) was added to the peritubular bath containing 145 mM Na. Fluid absorption (Jv), transepithelial unidirectional Na efflux (JNa 1 leads to b), and Na influx (JNa b leads to 1) were measured. Lowering peritubular [Na] inhibited JNa 1 leads to b by 28% and Jv by 61% of the control values. The degree of inhibition of Jv by low peritubular [Na] was dependent on the concentration of ultrafilterable calcium ([Ca]UF) over the range of 0.2-1.0 mM: as perfusate and bath ultrafilterable calcium was reduced, there was an attenuation of the low [Na]-induced inhibition of Jv. Above 1.0 mM [Ca]UF no further increase in inhibition of Jv was observed. Quinidine in the bath inhibited Jv by 37% and JNa 1 leads to b by 28%; A 23187 reduced Jv by 37% and JNa 1 leads to b by 15%. These results are consistent with the view that cytosolic [Ca2+], in turn dependent on a Na-Ca exchange mechanism located at the basolateral cell membrane, regulates, in part, the rate of proximal tubular efflux of sodium, calcium, and water.


1978 ◽  
Vol 234 (5) ◽  
pp. F381-F385 ◽  
Author(s):  
J. Cardinal ◽  
D. Duchesneau

In order to study the effect of potassium on the renal tubule, proximal convoluted tubules were dissected from rabbit kidneys and perfused in vitro. Omitting potassium from both the perfusate and bath caused the rate of fluid absorption and the transtubular potential difference to fall to zero. This effect was due to the absence of potassium in the bathing medium since no change was observed when potassium was omitted from the perfusate only. With 0.5 and 1.0 meq/liter of potassium in the bath, there was still a significant decrease from control in both the potential difference and the rate of fluid absorption. With 2.5 meq/liter of potassium in the bath, the results did not differ from control. In further studies, tubules were perfused with 10 meq/liter of potassium in both perfusate and bath. There was no change in the potential difference of fluid absorption. These results are consistent with the view that active transtubular transport of sodium is linked to the influx of potassium into the cell at the peritubular membrane and that this is probably mediated by sodium-potassium-ATPase. Our results also suggest that the variations of potassium concentration in the physiological range do not affect proximal tubular function.


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