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• W2016261750 abstract "This study investigates the effect in rats of acute CdCl 2 (5 μM) intoxication on renal function and characterizes the transport of Ca 2+ , Cd 2+ , and Zn 2+ in the proximal tubule (PT), loop of Henle (LH), and terminal segments of the nephron (DT) using whole kidney clearance and nephron microinjection techniques. Acute Cd 2+ injection resulted in renal losses of Na + , K + , Ca 2+ , Mg 2+ , PO 4 −2 , and water, but the glomerular filtration rate remained stable. 45 Ca microinjections showed that Ca 2+ permeability in the DT was strongly inhibited by Cd 2+ (20 μM), Gd 3+ (100 μM), and La 3+ (1 mM), whereas nifedipine (20 μM) had no effect. 109 Cd and 65 Zn 2+ microinjections showed that each segment of nephron was permeable to these metals. In the PT, 95% of injected amounts of 109 Cd were taken up. 109 Cd fluxes were inhibited by Gd 3+ (90 μM), Co 2+ (100 μM), and Fe 2+ (100 μM) in all nephron segments. Bumetanide (50 μM) only inhibited 109 Cd fluxes in LH; Zn 2+ (50 and 500 μM) inhibited transport of 109 Cd in DT. In conclusion, these results indicate that 1) the renal effects of acute Cd 2+ intoxication are suggestive of proximal tubulopathy; 2) Cd 2+ inhibits Ca 2+ reabsorption possibly through the epithelial Ca 2+ channel in the DT, and this blockade could account for the hypercalciuria associated with Cd 2+ intoxication; 3) the PT is the major site of Cd 2+ reabsorption; 4) the paracellular pathway and DMT1 could be involved in Cd 2+ reabsorption along the LH; 5) DMT1 may be one of the major transporters of Cd 2+ in the DT; and 6) Zn 2+ is taken up along each part of the nephron and its transport in the terminal segments could occur via DMT1." @default.
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• W2016261750 date "2004-11-01" @default.
• W2016261750 modified "2023-09-23" @default.
• W2016261750 title "Acute study of interaction among cadmium, calcium, and zinc transport along the rat nephron in vivo" @default.
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• W2016261750 doi "https://doi.org/10.1152/ajprenal.00120.2004" @default.
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