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Acute study of interaction among cadmium, calcium, and zinc transport along the rat nephron in vivo

Unité Mixte de Recherche-Centre National de la Recherche Scientifique 6548, Université de Nice-Sophia Antipolis, 06108 Nice Cedex 2, France

Submitted 5 April 2004 ; accepted in final form 22 July 2004

This study investigates the effect in rats of acute CdCl₂ (5 µM) intoxication on renal function and characterizes the transport of Ca²⁺, Cd²⁺, and Zn²⁺ 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 Cd²⁺ injection resulted in renal losses of Na⁺, K⁺, Ca²⁺, Mg²⁺, PO₄^–2, and water, but the glomerular filtration rate remained stable. ⁴⁵Ca microinjections showed that Ca²⁺ permeability in the DT was strongly inhibited by Cd²⁺ (20 µM), Gd³⁺ (100 µM), and La³⁺ (1 mM), whereas nifedipine (20 µM) had no effect. ¹⁰⁹Cd and ⁶⁵Zn²⁺ microinjections showed that each segment of nephron was permeable to these metals. In the PT, 95% of injected amounts of ¹⁰⁹Cd were taken up. ¹⁰⁹Cd fluxes were inhibited by Gd³⁺ (90 µM), Co²⁺ (100 µM), and Fe²⁺ (100 µM) in all nephron segments. Bumetanide (50 µM) only inhibited ¹⁰⁹Cd fluxes in LH; Zn²⁺ (50 and 500 µM) inhibited transport of ¹⁰⁹Cd in DT. In conclusion, these results indicate that 1) the renal effects of acute Cd²⁺ intoxication are suggestive of proximal tubulopathy; 2) Cd²⁺ inhibits Ca²⁺ reabsorption possibly through the epithelial Ca²⁺ channel in the DT, and this blockade could account for the hypercalciuria associated with Cd²⁺ intoxication; 3) the PT is the major site of Cd²⁺ reabsorption; 4) the paracellular pathway and DMT1 could be involved in Cd²⁺ reabsorption along the LH; 5) DMT1 may be one of the major transporters of Cd²⁺ in the DT; and 6) Zn²⁺ is taken up along each part of the nephron and its transport in the terminal segments could occur via DMT1.

heavy metals; epithelial calcium channel; divalent metal transporter 1; kidney

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