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THIRST AND VOLUME, ELECTROLYTE HOMEOSTASIS
1Institut National de la Santé et de la Recherche Médicale U76, Institut National de Transfusion Sanguine, F-75015 Paris; 2Service de Biologie Cellulaire, CEA/Saclay, F-91191 Gif-sur-Yvette Cedex; 3Laboratoire de Physiologie de l'Environnement, Université Claude Bernard, Faculté de Médecine Grange-Blanche, F-69373 Lyon Cedex 8; and 4Assistance Publique-Hôpitaux de Paris, Hôpital Sainte-Perrine, F-75781 Paris, France
Submitted 17 April 2003 ; accepted in final form 14 August 2003
Aging is commonly associated with defective urine-concentrating ability. The present study examined how the kidney and the brain of senescent (30-mo-old) female WAG/Rij rats respond to dehydration induced by 2 days of water deprivation in terms of urea transporter (UT) 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 with adult (10-mo-old) rats. Senescent rats responded to dehydration similarly to adult rats by a sixfold 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 twofold together with a fourfold increase in aquaporin-4 abundance. Dehydration did not alter the abundance of these transporters.
papillary osmolality; urea transporter-A1, -A2, -A3, and -B1; aquaporin-4; vasopressin
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