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1 Institut National de Transfusion Sanguine, INSERM U76, Paris, 75015, France; CEA/Saclay, Gif-sur-Yvette, Service de Biologie Cellulaire, Cedex, 91191, France
2 Faculte de Medecine Grange-Blanche, Laboratoire de Physiologie de l'Environnement, Lyon, 69373, France
3 Assistance Publique-Hopitaux de Paris, Hopital Sainte-Perrine, Paris, 75781, France
4 CEA/Saclay, Gif-sur-Yvette, Service de Biologie Cellulaire, Cedex, 91191, France
* To whom correspondence should be addressed. E-mail: trinh{at}idf.inserm.fr.
Aging is commonly associated with defective urine concentrating ability. The present study examined how the kidney and the brain of senescent (30 month-old) female WAG/Rij rats respond to dehydration induced by 2 days of water deprivation, in terms of urea transporter regulation. In euhydrated situation, senescent rats exhibited similar vasopressin plasma level, but lower urine osmolality and papillary urea concentration, and markedly reduced kidney UT-A1, UT-A3, and UT-B1 abundances, compared to adult (10 month-old) rats. Senescent rats responded to dehydration similarly to adult rats by a 6-fold increase in vasopressin plasma level. Their papillary urea concentration was doubled, without however attaining that of dehydrated adult rats. Such an enhanced papillary urea sequestration occurred with a great fall of both UT-A1 and UT-A3 abundances in the tip of inner medulla, and an increased UT-A1 abundance in the base of inner medulla. UT-A2 and UT-B1 were unchanged. These data suggest that the inability of control and thirsted senescent rats to concentrate urine as much as their younger counterparts derives from lower papillary urea concentration. In aging brain, UT-B1 abundance was increased 2-fold together with a 4-fold increase in aquaporin-4 abundance. Dehydration did not alter the abundance of these transporters.
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