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1 Department of Pediatrics, University of Colorado Health Sciences Center, Denver, CO, USA; Department of Medicine, University of Colorado Health Sciences Center, Denver, CO, USA
2 Department of Medicine, University of Colorado Health Sciences Center, Denver, CO, USA
3 National Institutes of Health, Renal Mechanisms Section, National Heart, Lung, and Blood Institute, Bethesda, MD, USA
* To whom correspondence should be addressed. E-mail: Robert.Schrier{at}uchsc.edu.
Chronic primary polydipsia 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 polydipsia on water metabolism and renal aquaporin water channels and sodium and urea transporter abundance in rats. Primary polydipsia was induced in male Sprague-Dawley rats (POLY) by daily administration of 15 gm powdered rat chow mixed in 100 ml water for 10 days. Control rats (CTL) received 15 gm powdered rat chow per day and ad libitum drinking water. Rats were studied following this period prior to further intervention, and with a 36-h period of water deprivation in order 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 urine output (80 ± 1 vs. 11 ± 1 ml/day, p<0.0001) and decreased urine osmolality (159 ± 13 vs. 1365 ± 188 mOsm/kg H2O, p<0.001) as compared to CTL rats. These findings were accompanied by decreased inner medulla aquaporin (AQP)-2 protein abundance in POLY rats as compared to CTL rats prior to water deprivation (76 ± 2 vs. 100 ± 7 % CTL mean, p<0.007). With water deprivation, maximal urinary osmolality was impaired in POLY rats vs. CTL rats (2404 ± 148 vs. 3286 ± 175 mOsm/kg H2O, 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 aquaporin (AQP)-2 protein abundance was decreased in POLY rats as 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 AQP3 or AQP4 or sodium and urea transporters. We conclude that the impaired urinary concentrating ability associated with primary polydipsia in rats is due to impaired osmotic equilibration in the collecting duct which is mediated primarily by decreased AQP2 protein abundance.
This article has been cited by other articles:
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  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]
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