ATP-dependent strontium uptake by basolateral membrane vesicles from rat renal cortex in the absence or presence of calcium

1992 ◽  
Vol 34 (1) ◽  
pp. 45-54 ◽  
Author(s):  
Naoko Sugihira ◽  
Yasunobu Aoki ◽  
Kazuo T. Suzuki
1990 ◽  
Vol 123 (4) ◽  
pp. 438-444 ◽  
Author(s):  
Yusuke Tsukamoto ◽  
Teiichi Tamura ◽  
Michiyo Saitoh ◽  
Yumiko Takita ◽  
Toshiaki Nakano

Abstract. To examine the hormonal regulation of the ATP-dependent Ca2+ pump in the kidneys, the ATP-dependent Ca2+ uptake by the basolateral membrane vesicles in the renal cortex was measured using radioactive calcium (45Ca2+) in rats with vitamin D deficiency or rats undergoing thyroparathyroidectomy. The Vmax of the Ca2+ pump activity was increased not only by administering calcitriol, but also by normalizing the serum calcium level in vitamin D-deficient rats. PTH suppressed the Ca2+ pump activity in normocalcemic vitamin D-deficient rats. Thyroparathyroidectomy did not affect the Ca2+ pump activity in the kidneys of normal rats. It was concluded that the ATP-dependent Ca2+ pump activity was depressed by secondary hyperparathyroidism in vitamin D-deficient rats.


1987 ◽  
Vol 252 (5) ◽  
pp. F883-F889 ◽  
Author(s):  
J. Eveloff ◽  
D. G. Warnock

The transport pathways for chloride in basolateral membrane vesicles from the rabbit renal cortex were investigated. 36Cl uptake was stimulated by the presence of potassium in the uptake media compared with sodium or N-methyl-D-glucamine. In addition, potassium (86Rb) uptake was stimulated more by chloride than by nitrate or gluconate. Neither of these processes was further stimulated by potassium gradients plus valinomycin, suggesting the presence of an electrically neutral K-Cl cotransport system. A magnesium-induced chloride conductance was also found in the basolateral membrane vesicles. In the absence of magnesium, the chloride conductance was low; valinomycin and an inwardly directed potassium gradient did not stimulate 36Cl uptake, anthracene-9-carboxylic acid did not inhibit 36Cl uptake, and valinomycin did not stimulate chloride-dependent 86Rb uptake. However, in the presence of 1 mM magnesium, opposite results were obtained; valinomycin and an inwardly directed potassium gradient stimulated 36Cl uptake, anthracene-9-carboxylic acid inhibited 36Cl uptake, and valinomycin stimulated chloride-dependent 86Rb uptake. Therefore, an electrically neutral K-Cl cotransport and magnesium-induced chloride conductance were found in renal cortical basolateral membrane vesicles prepared from the rabbit renal cortex.


1985 ◽  
Vol 248 (4) ◽  
pp. F574-F584 ◽  
Author(s):  
R. G. Abramson ◽  
M. S. Lipkowitz

[2-14C]Urate uptake and efflux were studied in brush border and basolateral membrane vesicles of rat renal cortex that were exposed to 20 microM copper chloride. In the presence of inwardly directed NaCl gradients urate uptake was maintained at levels in excess of chemical equilibrium. Comparison of glucose and chloride uptakes revealed that equilibrium glucose uptake was not affected by copper, but chloride failed to reach equilibrium in copper-exposed vesicles. It is suggested that the persistence of an electrolyte gradient could provide a driving force to raise the concentration of free intravesicular urate above that in the media. Preincubation of vesicles with unlabeled urate failed to diminish uptake of added urate; rather, urate uptake was trans stimulated. Uptake of labeled urate was also significantly accelerated when an outward gradient for unlabeled urate was created. Pyrazinoic and oxonic acids also trans stimulated urate uptake. The demonstration of accelerated homeo- and heteroexchange diffusion indicates that transport is carrier mediated in both brush border and basolateral vesicles. Outwardly directed hydroxyl gradients failed to influence urate uptake in either the presence or absence of copper or NaCl. Thus, this carrier, which is active only in the presence of trace amounts of copper, is distinct from a urate/anion exchanger.


1984 ◽  
Vol 246 (5) ◽  
pp. F663-F669 ◽  
Author(s):  
S. J. Schwab ◽  
S. Klahr ◽  
M. R. Hammerman

To ascertain whether Na+ gradient-stimulated 32Pi uptake was demonstrable in renal basolateral membrane vesicles, we measured 32Pi uptake in basolateral membrane suspensions isolated from canine renal cortex and compared solute uptake in basolateral suspensions with that measured in brush border suspensions. Measurements revealed Na+ gradient-dependent 32Pi transport in basolateral preparations. D-[3H] Glucose uptakes in basolateral suspensions were not stimulated by the Na+ gradient in contrast to findings in brush border suspensions. Na+ gradient-dependent 32Pi transport in basolateral suspensions was electrogenic in contrast to that measured in brush border preparations. Unlike 32Pi uptake in brush border preparations, Na+ gradient-dependent 32Pi uptake in basolateral suspensions did not increase as extravesicular pH was increased from 6.5 to 7.5. Na+ gradient-dependent 32Pi uptake in basolateral membranes showed saturation over the range of [Pi] from 5 to 100 microM (apparent Km, 14 +/- 2 microM; apparent Vmax, 34 +/- 2 pmol Pi X mg protein-1 X 30s-1). Our findings are compatible with the presence of an electrogenic Na+-Pi cotransporter in the canine proximal tubular basolateral membrane.


1982 ◽  
Vol 242 (2) ◽  
pp. F158-F170 ◽  
Author(s):  
R. G. Abramson ◽  
V. F. King ◽  
M. C. Reif ◽  
E. Leal-Pinto ◽  
S. B. Baruch

[2-14C]Urate uptake was studied in brush border and basolateral membrane vesicles of rat renal cortex. In the absence of copper, urate equilibrated without metabolism of transported urate. Exposure of the vesicles to copper significantly stimulated uptake, and in these vesicles uptake was also stimulated by NaCl or KCl gradients. Allantoin accumulated in these vesicles due to oxidation of transported urate. This oxidation is ascribed to a copper-stimulated, membrane-associated uricase since purified uricase and the membranes had similar Km values, both were inhibited by oxonic acid, and extramembranal uricase was not detected. Oxonic acid and pyrazinoic acid inhibited both uptake and enzyme activity. These findings suggest that urate uptake is carrier mediated and that uricase may play some role in transport. In addition, it appears that a significant loss of copper occurs during isolation of membrane vesicles that profoundly affects the characteristics of urate uptake. Those properties of the membrane that influence urate uptake, however, can be restored by exposure of the membranes to copper.


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