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1 National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892; and 2 Departments of Medicine and Physiology, Cardiovascular Research Institute, University of California, San Francisco, California 94143-0521
To examine the role of aquaporin-1
(AQP1) in near-isosmolar fluid reabsorption in the proximal tubule, we
compared osmolalities in micropuncture samples of late proximal tubular
fluid and plasma in wild-type (+/+) and AQP1-knockout (
/)
mice. Compared with matched wild-type mice, the / animals
produce a relatively hypotonic urine (607 ± 42 vs. 1,856 ± 101 mosmol/kgH2O) and have a higher plasma osmolality under
micropuncture conditions (346 ± 11 vs. 318 ± 5 mosmol/kgH2O; P < 0.05).
Measurements of tubular fluid osmolality were done in three groups of
mice, +/+, /, and hydrated / mice in which
plasma osmolality was reduced to 323 ± 1 mosmol/kgH2O. Late proximal tubular fluid osmolalities were 309 ± 5 (+/+, n = 21), 309 ± 4 (/, n = 24), and 284 ± 3 mosmol/kgH2O (hydrated /, n = 19). Tubular fluid chloride concentration averaged 152 ± 1 (+/+), 154 ± 1 (/), and 140 ± 1 mM (hydrated /).
Transtubular osmotic gradients in untreated and hydrated AQP1
/ mice were 39 ± 4 (n = 25) and 39 ± 3 mosmol/kgH2O (n = 19), values significantly higher
than in +/+ mice (12 ± 2 mosmol/kgH2O; n = 24;
both P < 0.001). AQP1 deficiency in mice generates marked
luminal hypotonicity in proximal tubules, resulting from the retrieval
of a hypertonic absorbate and indicating that near-isosmolar fluid
absorption requires functional AQP1.
water transport; kidney; micropuncture
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