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Recent data suggest possible net transport of urinary constituents across mammalian urinary tract epithelia (urothelia). To evaluate the effect of animal hydration status on such transport, we instilled urine collected during 2-day water deprivation, water loading, or ad libitum water intake into isolated in situ bladder(s) of groups of rats undergoing one of the same three hydration states. After 1-h bladder dwell, we retrieved the urine and measured differences in volume and solute concentrations between instilled and retrieved urine. We previously reported results regarding changes in urine volume and net urea and creatinine transport and herein report the results of net urinary sodium, potassium, and chloride transport in the same animals. During water-loading conditions, urinary concentrations of Na, K, and Cl rose 4.9 (30.7%), 2.6 (16.5%), and 6.0 meq/l (26.8%), respectively, indicating urothelial secretion into urine. During ad libitum water intake, urinary K and Cl concentrations fell 33.6 (14.8%) and 28.4 meq/l (12%), respectively (Na did not change), and during water deprivation urine Na, K, and Cl concentrations fell dramatically by 53.2 (18.6%), 159.4 (34.6%) and 133.7 meq/l (33.8%), respectively, reflecting urothelial reabsorption of each ion. For each ionic species, two factors independently influenced transport: instilled urinary ion concentration and animal hydration state. These results demonstrate significant regulated ion transport across mammalian urothelia, support the notion that lower urinary tract modifies final urine, and suggest that the lower urinary tract may play a role in local and whole animal solute homeostasis. [ABSTRACT FROM AUTHOR]

Although mammalian urinary tract epithelium (urothelium) is generally considered impermeable to water and solutes, recent data suggest that urine constituents may be reabsorbed during urinary tract transit and storage. To study water and solute transport across the urothelium in an in vivo rat model, we instilled urine (obtained during various rat hydration conditions) into isolated in situ rat bladders and, after a 1-h dwell, retrieved the urine and measured the differences in urine volume and concentration and total quantity of urine urea nitrogen and creatinine between instilled and retrieved urine in rat groups differing by hydration status. Although urine volume did not change >1.9% in any group, concentration (and quantity) of urine urea nitrogen in retrieved urine fell significantly (indicating reabsorption of urea across bladder urothelia), by a mean of 18% (489 mg/dl, from an instilled 2,658 mg/dl) in rats receiving ad libitum water and by a mean of 39% (2,544 mg/dl, from an instilled 6,204 mg/dl) in water-deprived rats, but did not change (an increase of 15 mg/dl, P = not significant, from an instilled 300 mg/dl) in a water-loaded rat group. Two separate factors affected urea nitrogen reabsorption rates, a urinary factor related to hydration status, likely the concentration of urea nitrogen in the instilled urine, and a bladder factor(s), also dependent on the animal's state of hydration. Urine creatinine was also absorbed during the bladder dwell, and hydration group effects on the concentration and quantity of creatinine reabsorbed were qualitatively similar to the hydration group effect on urea transport. These findings support the notion(s) that urinary constituents may undergo transport across urinary tract epithelia, that such transport may be physiologically regulated, and that urine is modified during transit and storage through the urinary tract. [ABSTRACT FROM AUTHOR]

There is increasing evidence that mammalian urinary tract epithelial cells utilize membrane channels and transporters to transport solutes across their apical (luminal) and basalateral membranes to modify solute concentrations in both cell and urine. This study investigates the expression, localization, and regulation of the ROMK (Kir 1.1) potassium channels in rat and dog ureter and bladder tissues. Immunoblots of homogenates of whole ureter, whole bladder, bladder epithelial cells, and bladder smooth muscle tissues in both rat and dog identified ∼45- to 50-kDa bands characteristic of ROMK in all tissues. RT-PCR identified ROMK mRNA in these same tissues in both animal species. ROMK protein localized by immunocytochemistry was strongly expressed in the apical membranes of the large umbrella cells lining the bladder lumen and to a lesser extent in the cytoplasm of epithelial cells and smooth muscle cells in the rat bladder. ROMK protein and mRNA were also discovered in cardiac, striated, and smooth muscle in diverse organs. There was no difference in immunoblot expression of ROMK abundance in bladder homogenates (whole bladder, epithelial cell, or muscle cell) or ureteral homogenates between groups of rats fed high- or low-potassium diets. Although the functional role of ROMK in urinary tract epithelia and smooth muscle is unknown, ROMK may participate in the regulation of epithelial and smooth muscle cell volume and osmolality, in the dissipation of potassium leaked or diffused from urine across the epithelial cell apical membranes or tight junctions, and in net or bidirectional potassium transport across urinary tract epithelia. [ABSTRACT FROM AUTHOR]