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EDITORIAL FOCUS

ANG II provokes acute trafficking of distal tubule Na⁺-Cl^– cotransporter to apical membrane

¹Department of Physiology and Biophysics, University of Southern California Keck School of Medicine, Los Angeles, California; and ²The Water and Salt Research Center, Department of Cell Biology, Institute of Anatomy, University of Aarhus, Aarhus, Denmark

Submitted 10 February 2007 ; accepted in final form 9 May 2007

The distal convoluted tubule (DCT) Na⁺-Cl^– cotransporter (NCC), the target of thiazide diuretics, is responsible for the reabsorption of 5–10% of filtered NaCl. The aim of this study was to test the hypothesis that acute infusion of the angiotensin-converting enzyme (ACE) inhibitor captopril (at 12 µg/min) for 20 min provokes trafficking of NCC from apical plasma membranes (APM) to subapical cytoplasmic vesicles (SCV), which is reversed by acute ANG II infusion (ANG II at 20 ng·kg^–1·min^–1 along with 12 µg/min captopril) for 20 min in male Sprague-Dawley rats (250–350 g). By immuno-electron microscopy using an anti-NCC (D. Ellison) 71.5 ± SD 4.9% of the NCC gold labeling was associated with the APM in control, sham operated, and infused rats, while captopril infusion reduced NCC in APM to 54.9 ± 6.9% (P < 0.001) and markedly increased immunogold labeling of SCV. Subsequent infusion of ANG II with captopril restored NCC immunogold labeling of APM to 72.4 ± 4.2%, that is, 20% of the total NCC trafficked between APM and SCV. Likewise, on density gradients of cortex, captopril provoked redistribution of 27.3% of total NCC from low-density APM-enriched membranes to higher-density membranes and ANG II+captopril restored 20.3% of the NCC to APM-enriched fractions. Redistribution occurred independent of a change in NCC total abundance. In conclusion, this study demonstrates that ACE inhibition provokes acute trafficking of NCC out of the plasma membrane, which likely decreases DCT Na⁺ reabsorption, while ANG II provokes rapid trafficking of NCC from stores in subapical vesicles to the plasma membrane, which likely increases DCT Na⁺ reabsorption.

sodium transport; thiazide receptor; immunoelectron microscopy

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