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1 Department of Medicine, Division of Endocrinology and Metabolism, Georgetown University, Washington DC 20007, USA
2 Department of Physiology, University of Occupational and Environmental Health, Kitakyushu, Japan
* To whom correspondence should be addressed. E-mail: tiany{at}georgetown.edu.
Renal concentrating ability is known to be impaired with aging. The antidiuretic hormone, vasopressin (AVP), plays an important role in renal water excretion by regulating the membrane insertion and abundance of the water channel, aquaporin-2 (AQP2); this effect is primarily mediated via the V2 subtype of the AVP receptor (V2R). This study evaluated the hypothesis that decreased renal sensitivity to AVP, with subsequent altered renal AQP2 expression, contributes to the reduced urine concentrating ability with aging. Our results show that under baseline conditions, urine osmolality is significantly lower in aged F344BN hybrid rats despite equivalent plasma AVP concentrations as in young rats. Levels of kidney V2R mRNA expression and AQP2 abundances were also significantly decreased in aged F344BN rats, as was AQP2 immunostaining in collecting duct cells . In response to moderate water restriction, urine osmolality increased by significantly lesser amounts in aged F344BN rats compared to young rats despite similar increases in plasma AVP levels. Moderate water restriction induced equivalent relative increases in renal AQP2 abundances in all age groups, but resulted in significantly lower abundances in total kidney AQP2 protein in aged compared to young F344BN rats. These results therefore demonstrate a functional impairment of renal concentrating ability in aged F344BN rats that is not due to impaired secretion of AVP, but rather appears to be related to impaired responsiveness of the kidney to AVP that is secondary, at least in part, to a down-regulation of renal V2R expression and AQP2 abundance.
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