Document Detail


Acute hypertension provokes acute trafficking of distal tubule Na-Cl cotransporter (NCC) to subapical cytoplasmic vesicles.
MedLine Citation:
PMID:  19144688     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
When blood pressure (BP) is elevated above baseline, a pressure natriuresis-diuresis response ensues, critical to volume and BP homeostasis. Distal convoluted tubule Na(+)-Cl(-) cotransporter (NCC) is regulated by trafficking between the apical plasma membrane (APM) and subapical cytoplasmic vesicles (SCV). We aimed to determine whether NCC trafficking contributes to pressure diuresis by decreasing APM NCC or compensates for increased volume flow to the DCT by increasing APM NCC. BP was raised 50 mmHg (high BP) in rats by arterial constriction for 5 or 20-30 min, provoking a 10-fold diuresis at both times. Kidneys were excised, and NCC subcellular distribution was analyzed by 1) sorbitol density gradient fractionation and immunoblotting and 2) immunoelectron microscopy (immuno-EM). NCC distribution did not change after 5-min high BP. After 20-30 min of high BP, 20% of NCC redistributed from low-density, APM-enriched fractions to higher density, endosome-enriched fractions, and, by quantitative immuno-EM, pool size of APM NCC decreased 14% and SCV pool size increased. Because of the time lag of the response, we tested the hypothesis that internalization of NCC was secondary to the decrease in ANG II that accompanies high BP. Clamping ANG II at a nonpressor level by coinfusion of captopril (12 microg/min) and ANG II (20 ng.kg(-1).min(-1)) during 30-min high BP reduced diuresis to eightfold and prevented redistribution of NCC from APM- to SCV-enriched fractions. We conclude that DCT NCC may participate in pressure natriuresis-diuresis by retraction out of apical plasma membranes and that the retraction is, at least in part, driven by the fall in ANG II that accompanies acute hypertension.
Authors:
Donna H Lee; Anne D M Riquier; Li E Yang; Patrick K K Leong; Arvid B Maunsbach; Alicia A McDonough
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't     Date:  2009-01-14
Journal Detail:
Title:  American journal of physiology. Renal physiology     Volume:  296     ISSN:  1931-857X     ISO Abbreviation:  Am. J. Physiol. Renal Physiol.     Publication Date:  2009 Apr 
Date Detail:
Created Date:  2009-03-23     Completed Date:  2009-06-02     Revised Date:  2013-06-02    
Medline Journal Info:
Nlm Unique ID:  100901990     Medline TA:  Am J Physiol Renal Physiol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  F810-8     Citation Subset:  IM    
Affiliation:
Dept. of Cell and Neurobiology, Univ. of Southern California Keck School of Medicine, 1333 San Pablo St., BMT 403, Los Angeles, CA 90089, USA.
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MeSH Terms
Descriptor/Qualifier:
Acute Disease
Angiotensin II / administration & dosage
Angiotensin-Converting Enzyme Inhibitors / administration & dosage
Animals
Blood Pressure* / drug effects
Captopril / administration & dosage
Cell Fractionation
Cell Membrane / drug effects,  metabolism*,  ultrastructure
Cytoplasmic Vesicles / drug effects,  metabolism*,  ultrastructure
Disease Models, Animal
Diuresis* / drug effects
Hypertension / metabolism*,  physiopathology
Infusions, Intravenous
Kidney Tubules, Distal / drug effects,  metabolism*,  ultrastructure
Male
Microscopy, Immunoelectron
Protein Transport
Rats
Rats, Sprague-Dawley
Receptors, Drug / metabolism*
Sodium Chloride Symporters / metabolism*
Symporters / metabolism*
Time Factors
Grant Support
ID/Acronym/Agency:
DK-34316/DK/NIDDK NIH HHS; HL-085388/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/Angiotensin-Converting Enzyme Inhibitors; 0/Receptors, Drug; 0/Slc12a3 protein, rat; 0/Sodium Chloride Symporters; 0/Symporters; 11128-99-7/Angiotensin II; 62571-86-2/Captopril
Comments/Corrections

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