AJP - Renal Journal of Applied Physiology
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

Am J Physiol Renal Physiol 282: F1120-F1128, 2002. First published January 8, 2002; doi:10.1152/ajprenal.00266.2001
0363-6127/02 $5.00
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow All Versions of this Article:
282/6/F1120    most recent
00266.2001v1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in ISI Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via ISI Web of Science (10)
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Frank, A. E.
Right arrow Articles by Weiner, I. D.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Frank, A. E.
Right arrow Articles by Weiner, I. D.
Vol. 282, Issue 6, F1120-F1128, June 2002

Mechanisms through which ammonia regulates cortical collecting duct net proton secretion

Amy E. Frank1, Charles S. Wingo1, Peter M. Andrews2, Shana Ageloff3, Mark A. Knepper3, and I. David Weiner1

1 Division of Nephrology, Hypertension, and Transplantation, University of Florida, and Gainesville Veterans Affairs Medical Center, Gainesville, Florida 32610-0224; 2 Department of Cell Biology, Georgetown University, Washington, District of Columbia 20007; and 3 Laboratory of Kidney and Electrolyte Metabolism, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland 20892

Ammonia stimulates cortical collecting duct (CCD) net bicarbonate reabsorption by activating an apical H+-K+-ATPase through mechanisms that are independent of ammonia's known effects on intracellular pH and active sodium transport. The present studies examined whether this stimulation occurs through soluble N-ethylmaleimide-sensitive fusion attachment receptor (SNARE) protein-mediated vesicle fusion. Rabbit CCD segments were studied using in vitro microperfusion, and transepithelial bicarbonate transport was measured using microcalorimetry. Ammonia's stimulation of bicarbonate reabsorption was blocked by either chelating intracellular calcium with 1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid acetoxymethyl ester or by inhibiting microtubule polymerization with colchicine compared with parallel studies performed in the absence of these inhibitors. An inactive structural analog of colchicine, lumicolchicine, did not alter ammonia's stimulation of bicarbonate reabsorption. Tetanus toxin, a zinc endopeptidase specific for vesicle-associated SNARE (v-SNARE) proteins, prevented ammonia from stimulating net bicarbonate reabsorption. Consistent with the functional evidence for v-SNARE involvement, antibodies directed against a conserved region of isoforms 1-3 of the tetanus toxin-sensitive, vesicle-associated membrane protein (VAMP) members of v-SNARE proteins labeled the apical and subapical region of collecting duct intercalated cells. Similarly, antibodies to NSF protein, a protein involved in activation of SNARE proteins for subsequent vesicle fusion, localized to the apical and subapical region of collecting duct intercalated cells. These results indicate that ammonia stimulates CCD bicarbonate reabsorption through an intracellular calcium-dependent, microtubule-dependent, and v-SNARE-dependent mechanism that appears to involve insertion of cytoplasmic vesicles into the apical plasma membrane of CCD intercalated cells.

intracellular calcium; 1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid acetoxymethyl ester; microtubule; soluble N-ethylmaleimide-sensitive fusion attachment receptor protein; hydrogen-potassium-adenosine triphosphatase


This article has been cited by other articles:


Home page
 Am. J. Physiol. Renal Physiol.Home page
H.-W. Lee, J. W. Verlander, J. M. Bishop, P. Igarashi, M. E. Handlogten, and I. D. Weiner
Collecting duct-specific Rh C glycoprotein deletion alters basal and acidosis-stimulated renal ammonia excretion
Am J Physiol Renal Physiol, June 1, 2009; 296(6): F1364 - F1375.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Renal Physiol.Home page
I. J. Lynch, A. Rudin, S.-L. Xia, L. R. Stow, G. E. Shull, I. D. Weiner, B. D. Cain, and C. S. Wingo
Impaired acid secretion in cortical collecting duct intercalated cells from H-K-ATPase-deficient mice: role of HK{alpha} isoforms
Am J Physiol Renal Physiol, March 1, 2008; 294(3): F621 - F627.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Renal Physiol.Home page
D.-O. D. Mak, B. Dang, I. D. Weiner, J. K. Foskett, and C. M. Westhoff
Characterization of ammonia transport by the kidney Rh glycoproteins RhBG and RhCG
Am J Physiol Renal Physiol, February 1, 2006; 290(2): F297 - F305.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Renal Physiol.Home page
M. E. Handlogten, S.-P. Hong, C. M. Westhoff, and I. D. Weiner
Apical ammonia transport by the mouse inner medullary collecting duct cell (mIMCD-3)
Am J Physiol Renal Physiol, August 1, 2005; 289(2): F347 - F358.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Renal Physiol.Home page
J. W. Verlander, R. T. Miller, A. E. Frank, I. E. Royaux, Y.-H. Kim, and I. D. Weiner
Localization of the ammonium transporter proteins RhBG and RhCG in mouse kidney
Am J Physiol Renal Physiol, February 1, 2003; 284(2): F323 - F337.
[Abstract] [Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Visit Other APS Journals Online