HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) All Versions of this Article: 285/5/F965    most recent 00085.2003v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via ISI Web of Science (6) Citing Articles via Google Scholar Google Scholar Articles by Cadnapaphornchai, M. A. Articles by Schrier, R. W. Search for Related Content PubMed PubMed Citation Articles by Cadnapaphornchai, M. A. Articles by Schrier, R. W.

Effect of primary polydipsia on aquaporin and sodium transporter abundance

Departments of ¹Medicine and ²Pediatrics, University of Colorado School of Medicine, Denver, Colorado 80262; and ³Renal Mechanisms Section, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland 20892-1603

Submitted 4 March 2003 ; accepted in final form 11 July 2003

Chronic primary polydipsia (POLY) in humans is associated with impaired urinary concentrating ability. However, the molecular mechanisms responsible for this finding have not been elucidated. The purpose of this study was to examine the effect of chronic primary POLY on water metabolism and renal aquaporin (AQP) water channels and sodium and urea transporter abundance in rats. Primary POLY was induced in male Sprague-Dawley rats by daily administration of 15 g powdered rat chow mixed in 100 ml water for 10 days. Control rats (CTL) received 15 g powdered rat chow per day and ad libitum drinking water. Rats were studied following this period before further intervention and with a 36-h period of water deprivation to examine maximal urinary concentrating ability. At baseline, POLY rats demonstrated significantly greater water intake (100 ± 1 vs. 22 ± 2 ml/day, P < 0.0001) and urinary output (80 ± 1 vs. 11 ± 1 ml/day, P < 0.0001) and decreased urinary osmolality (159 ± 13 vs. 1,365 ± 188 mosmol/kgH₂O, P < 0.001) compared with CTL rats. These findings were accompanied by decreased inner medulla AQP-2 protein abundance in POLY rats compared with CTL rats before water deprivation (76 ± 2 vs. 100 ± 7% CTL mean, P < 0.007). With water deprivation, maximal urinary osmolality was impaired in POLY vs. CTL rats (2,404 ± 148 vs. 3,286 ± 175 mosmol/kgH₂O, P < 0.0005). This defect occurred despite higher plasma vasopressin concentrations and similar medullary osmolalities in POLY rats. In response to 36-h water deprivation, inner medulla AQP-2 protein abundance was decreased in POLY rats compared with CTL rats (65 ± 5 vs. 100 ± 5% CTL mean, P < 0.0006). No significant differences were noted in renal protein abundance of either AQP-3 or AQP-4 or sodium and urea transporters. We conclude that the impaired urinary concentrating ability associated with primary POLY in rats is due to impaired osmotic equilibration in the collecting duct that is mediated primarily by decreased AQP-2 protein abundance.

urinary concentrating ability

This article has been cited by other articles:

				R. W. Schrier Body Water Homeostasis: Clinical Disorders of Urinary Dilution and Concentration J. Am. Soc. Nephrol., July 1, 2006; 17(7): 1820 - 1832. [Full Text] [PDF]