Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P41181 (collecting duct)
 5,183 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

D-Glucose is an important substrate of energy metabolism and osmolyte synthesis in the renal papillary collecting duct. In order to characterize the cellular entry of D-glucose in this tubular segment, collecting duct cells were isolated from rat kidney papilla and the rate of D-glucose uptake was measured indirectly by monitoring the D-glucose-dependent O2 uptake in the presence of the uncoupler CCCP. D-Glucose uptake was found to be sodium-independent and not sensitive to phlorizin even at a concentration of 10(-3) M. Uptake was, however, completely inhibited by 10(-5) M cytochalasin B and 10(-4) M phloretin. The apparent Ki for cytochalasin B was 1.5 x 10(-6) M and for phloretin 2.0 x 10(-5) M. Studies on the substrate specificity revealed that at 1 mM D-mannose is taken up and metabolized to the same extent as D-glucose. A 50-fold higher concentration of 2-deoxy-D-glucose and 2-amino-2-deoxy-D-glucose inhibited D-glucose uptake completely whereas alpha-methyl-D-glucoside, D-allose, and D-galactose were without effect. Under conditions where D-glucose utilization was maximally stimulated an apparent Km of 1.2 mM and a Vmax of 1 mmol D-glucose/g protein.hour was found for D-glucose uptake. These results indicate that the D-glucose uptake into papillary collecting duct cells is probably mediated by a transport system similar to the one found in basal-lateral membranes of polarized renal, intestinal, and liver cells as well as in nonpolarized fat cells and erythrocytes.
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PMID:Sugar transport in isolated rat kidney papillary collecting duct cells. 321 25

Cisplatin (CP) nephrotoxicity in vivo is characterized by proximal tubule (PT) and collecting duct dysfunction. We reported previously that mitochondrial injury is an important early event in CP toxicity to PT cells and precedes inhibition of Na+,K(+)-ATPase activity and loss of cell K+. In the present study, we monitored oxygen consumption (QO2) and net K+ fluxes in intact inner medullary collecting duct (IMCD) and PT cells in vitro, using O2- and K(+)-sensitive electrodes, to determine if CP has similar effects on IMCD cells. Short-term exposure of IMCD cells to CP resulted in inhibition of spontaneous, ouabain-sensitive and ouabain-oversensitive QO2, but to a lesser degree than in PT. Ouabain-sensitive K+ transport and cell K+ content were also reduced in intact IMCD cells in this setting, confirming inhibition of Na+,K(+)-ATPase activity. In contrast, Na+,K(+)-ATPase activity measured in IMCD cell lysates was not altered. These results suggested that CP inhibited Na+,K(+)-ATPase activity in intact IMCD cells indirectly either by blocking Na+ entry or by inhibiting mitochondrial oxidative phosphorylation. Nystatin (Na+ ionophore) and carbonyl cyanide m-chlorophenylhydrazone (CCCP, uncoupler of oxidative phosphorylation) were used to distinguish between these possibilities. Nystatin-stimulated and CCCP-uncoupled QO2 were reduced in CP-treated IMCD cells by 34 +/- 10% and 25 +/- 5%, respectively, indicating mitochondrial injury. Again, the effects of CP on nystatin-stimulated and CCCP-uncoupled QO2 in IMCD cells were significantly less dramatic than in PT cells.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Differential actions of cisplatin on renal proximal tubule and inner medullary collecting duct cells. 838 66