scholarly journals Na+-gradient-dependent stimulation of renal transport of ρ-aminohippurate

1982 ◽  
Vol 208 (1) ◽  
pp. 243-246 ◽  
Author(s):  
M I Sheikh ◽  
J V Møller

Transport of rho-aminohippurate was studied by the use of a preparation of rabbit kidney basolateral-membrane vesicles and in rat kidney-cortex slices under anaerobic conditions. With both preparations clear evidence of Na+-gradient stimulation of rho-aminohippurate transport (‘overshoot’) was obtained. These results thus indicate that a significant aspect of active rho-aminohippurate transport is by co-transport with Na+, and they appear to resolve previous disagreements concerning the role of Na+. Vesicle studies with a potential-sensitive dye suggested that rho-aminohippurate may be transported electroneutrally, i.e. in a 1:1 complex with Na+.

1958 ◽  
Vol 195 (2) ◽  
pp. 343-346 ◽  
Author(s):  
E. J. Støren

Active uptake of PAH by rat renal cortex slices was studied by the method of Cross and Taggart. Uptake was determined at low and at high medium concentrations of PAH. Pentobarbital sodium in concentrations comparable to those found in plasma during anesthesia, significantly depressed the uptake of PAH on all occasions. Simultaneously oxygen consumption was reduced. Acetate failed to stimulate PAH uptake in the presence of pentobarbital, although tissue respiration was restored to normal.


1984 ◽  
Vol 67 (5) ◽  
pp. 529-534 ◽  
Author(s):  
P. K. Wirdnam ◽  
R. D. G. Milner

1. Rat kidney cortex slices were incubated for 30 min at 37°C in unmodified Krebs-Henseleit buffer containing aldosterone, vasopressin, theophylline, ethacrynic acid, frusemide, spironolactone or ouabain. 2. Tamm—Horsfall glycoprotein (THG) released into the media was measured by radioimmunoassay and at the end of each experiment the slices were homogenized and assayed for THG content. 3. Incubation of kidney cortex slices in unmodified buffer resulted in a significant increase in the slice THG content when compared with pre-incubation levels. The increase was prevented by puromycin or cycloheximide. 4. Incubation in ethacrynic acid (1 mmol/l) or frusemide (10 mmol/l) resulted in a significant increase in release of THG when compared with unmodified buffer. Puromycin or cycloheximide failed to prevent the increased release. 5. THG release induced by ethacrynic acid or frusemide is probably the result of an aggregation-disaggregation reaction on the cell membrane. It is suggested that the action of the chloride inhibiting diuretics, ethacrynic acid and frusemide, is mediated in some way via THG.


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