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Am J Physiol Renal Physiol (May 16, 2007). doi:10.1152/ajprenal.00064.2007
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Submitted on February 10, 2007
Accepted on May 9, 2007

Angiotensin II provokes acute trafficking of distal tubule NaCl cotransporter (NCC) to apical membrane

Monica B Sandberg1, Anne D.M. Riquier1, Kaarina Pihakaski-Maunsbach2, Alicia A. McDonough1, and Arvid B. Maunsbach3*

1 Department of Physiology and Biophysics, University of Southern California, Los Angeles, California, United States
2 The Water and Salt Research Center, University of Aarhus, Aarhus, Denmark
3 The Water and Salt Research Center, Institute of Anatomy, University of Aarhus, Aarhus, Denmark

* To whom correspondence should be addressed. E-mail: maunsbach{at}ana.au.dk.

The distal convoluted tubule Na+-Cl- cotransporter (NCC), the target of thiazide diuretics, is responsible for the reabsorption of 5 - 10% of filtered NaCl. This study tests the hypothesis that acute infusion of the 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 Angiotensin II infusion along with captopril for 20 min in male Sprague Dawley rats. By immunoelectron 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 AngII 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 AngII+ 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 AngII provokes rapid trafficking of NCC from stores in sub-apical vesicles to the plasma membrane, which likely increases DCT Na+ reabsorption.




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