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1 Department of Cell Biology, Institute of Anatomy, University of Aarhus, DK-8000 Aarhus C; 2 Department of Physiology, School of Medicine, Dongguk University, Kyungju 780 - 714, Korea; 3 School of Biomedical Sciences, University of Leeds, Leeds LS2 9NQ, United Kingdom; 4 Laboratory M (Diabetes and Endocrinology), Aarhus University Hospital, DK-8000 Aarhus C; 5 Laboratory of Kidney and Electrolyte Metabolism, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland 20892; and 6 Department of Clinical Physiology, Institute of Experimental Clinical Research, Aarhus University Hospital, DK-8200 Aarhus N, Denmark
Diabetes mellitus (DM) is associated with osmotic diuresis
and natriuresis. At day 15, rats with DM induced by
streptozotocin (n = 13) had severe hyperglycemia
(27.1 ± 0.4 vs. 4.7 ± 0.1 mM in controls) and had a
fivefold increase in water intake (123 ± 5 vs. 25 ± 2 ml/day) and urine output. Semiquantitative immunoblotting revealed a
significant increase in inner medullary AQP2 (201 ± 12% of
control rats, P < 0.05) and phosphorylated
(Ser256) AQP2 (p-AQP2) abundance (299 ± 32%) in DM
rats. Also, the abundance of inner medullary AQP3 was markedly
increased to 171 ± 19% of control levels (100 ± 4%,
n = 7, P < 0.05). In contrast, the
abundance of whole kidney AQP1 (90 ± 3%) and inner medullary
AQP4 (121 ± 16%) was unchanged in rats with DM. Immunoelectron
microscopy further revealed an increased labeling of AQP2 in the apical
plasma membrane of collecting duct principal cells (with less labeling in the intracellular vesicles) of DM rats, indicating enhanced trafficking of AQP2 to the apical plasma membrane. There was a marked
increase in urinary sodium excretion in DM. Only
Na+/H+ exchanger NHE3 was downregulated
(67 ± 10 vs. 100 ± 11%) whereas there were no significant
changes in abundance of type 2 Na-phosphate cotransporter (128 ± 6 vs. 100 ± 10%); the Na-K-2Cl cotransporter (125 ± 19 vs.
100 ± 10%); the thiazide-sensitive Na-Cl cotransporter (121 ± 9 vs. 100 ± 10%); the 
1-subunit of the
Na-K-ATPase (106 ± 7 vs. 100 ± 5%); and the proximal
tubule Na-HCO3 cotransporter (98 ± 16 vs. 100 ± 7%). In conclusion, DM rats had an increased AQP2, p-AQP2, and AQP3
abundance as well as high AQP2 labeling of the apical plasma membrane,
which is likely to represent a vasopressin-mediated compensatory
increase in response to the severe polyuria. In contrast, there were no
major changes in the abundance of AQP1, AQP4, and several major
proximal and distal tubule Na+ transporters except NHE3
downregulation, which may participate in the increased sodium excretion.
aquaporins; polyuria; sodium transport; urinary concentrating mechanism
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