Changes in composition of the urine in ureter and bladder at low urine flow

Levinsky, Norman G.; Berliner, Robert W.

doi:10.1152/ajplegacy.1959.196.3.549

Cited by 99 publications

(47 citation statements)

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“…It has been noted that the urothelium has very low permeability to several urinary solutes and substrates. Mammalian urothelium modifies urine concentration and composition by reabsorbing potassium (K + ), urea, and creatine and secreting sodium (Na + ) [11,12], and the composition of urine changes during its transport through urine passages from the renal pelvis to the urinary bladder, a finding showing a modifying function of the urothelium [11]. A dramatic example of net water or solute movement is in hibernating bears, which are capable of reabsorbing their entire daily urine production during the months of winter [13].…”

Section: Discussionmentioning

confidence: 99%

The Expression of AQP1 and eNOS in Menopausal Rat Urinary Bladder

et al. 2010

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Purpose: Aquaporins (AQPs) have been reported to be expressed in rat and human urothelium. Nitric oxide (NO) is thought to play an important role in the bladder overactivity related to menopause. The purpose of this study was to investigate the effect of hormonal alteration on the expression of AQP1 and eNOS in menopausal rat urinary bladder. Materials and Methods: Female Sprague-Dawley rats (230-240 g, N=30) were divided into three groups: control (N=10), bilateral ovariectomy (Ovx, N=10), and bilateral ovariectomy followed by subcutaneous injections of 17β -estradiol (50 mg/kg/day, Ovx+Est, N=10). After 4 weeks, urodynamic studies measuring the contraction interval and contraction pressure were done. The expression and cellular localization of AQP1 and eNOS were determined by performing Western blotting and immunohistochemistry on the rat urinary bladder. Results: The approximate contraction interval (min) was significantly decreased in the Ovx group (3.9±0.25) compared to the control group (6.7±0.15), and was increased after estrogen treatment (9.7±0.22) (p<0.05). The AQP1 and eNOS immunoreactivities were localized in the same areas: capillaries, arterioles, and venules of the lamina propria. The protein expression of AQP1 was not changed significantly, whereas eNOS expression was significantly decreased in the Ovx group and restored to the control value in the Ovx+Est group. Conclusions: This study showed that ovariectomy causes a significant change in e-NOS expression without a change in AQP1 in menopausal rat urinary bladder. This may imply that e-NOS has a functional role in the bladder overactivity that occurs in association with menopause.

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Section: Discussionmentioning

confidence: 99%

The Expression of AQP1 and eNOS in Menopausal Rat Urinary Bladder

et al. 2010

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“…Previous studies that examined net in vivo potassium flux in bladder and ureter have demonstrated potassium reabsorption down its concentration gradient from lumen (urine or artificial test solutions) to blood (8,16,27,34). Although the mechanism(s) of potassium reabsorption may, in part, be secondary to passive diffusion and or leak across the apical cell membrane or through tight junctions, in recent electrophysiological studies, Sun and coworkers (33) showed a strongly rectifying potassium current with conductive characteristics of the K ir 2.1 channel as well as the Maxi-K channel in normal cultured human bladder cells (33), and, in Ussing chamber experiments with rabbit bladder, Wang et al (35) demonstrated that increased mucosal hydraulic pressure led to increased sodium reabsorption (probably through ENaC) as well as potassium secretion, likely through a stretch-activated nonselective cation channel.…”

Section: Discussionmentioning

confidence: 99%

“…Given these considerations, it may not be surprising that net urothelial flux of multiple ionic and nonionic solutes, including urea (9,10,11,16,26,34), sodium (9,10,11,16,27,34,35), calcium (26), and potassium (16,27,34,35), has been described using a variety of in vivo and in vitro techniques in many animal species. In these experiments, fluxes usually occurred in the direction of the concentration gradient, but fluxes were influenced as well by urine pH (8), bladder volume (9), and hydrostatic pressure (35).…”

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confidence: 99%

The ROMK potassium channel is present in mammalian urinary tract epithelia and muscle

Spector¹,

Yang²,

Klopouh³

et al. 2008

American Journal of Physiology-Renal Physiology

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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 ϳ45-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. epithelial sodium channel; calponin MAMMALIAN URINARY TRACT EPITHELIA (urothelia) has long been held to serve solely as a storage conduct for urine made by the kidney and, in particular, to prevent modification of urine by inhibiting net flux of water and solutes across the epithelial cell luminal membrane (7). The barrier(s) preventing transepithelial flux of urine constituents have been shown to include: the lumenal membrane (containing unique uroplakin proteins) of the large ("umbrella") cells lining the urinary tract lumen (12), tight junctions adjoining the umbrella cells, and a glycosaminoglycans layer overlying and adjacent to the lumenal membrane (13, reviewed in Ref. 17). Evidence for the effectiveness of these barriers, which have been thought to be passive in nature and not to utilize or require membrane transporters, comes from Ussing chamber studies documenting very low urothelial permeability to water, ions, and nonelectrolytes and very high transepithelial cell resistance in stretched bladders and apical membrane endosomes obtained from rabbits under basal conditions (2, 24).However, although the permeabilities of urothelia for water and various urinary solutes may be low under basal conditions, urothelial permeabilities in animals subjected to dietary, physiological (e.g., water loading/water restricted), or other stress could be altered. Furthermore, urothelial cells are...

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“…Spector and coworkers (39) described high concentrations of urea (and creatinine) in both rat and dog bladder tissues; in rats, water deprivation increased tissue urea concentrations whereas water loading decreased tissue urea concentrations, suggesting that animal hydration status might regulate the magnitude of urothelial transport. Furthermore, several older in vivo studies have demonstrated net vectoral transport of water, ions, and solutes across epithelial membranes, usually down their concentration gradients, in several mammalial species (15,16,23,31,33,44,45,46). Levinsky and Berliner (23) reported loss of water, potassium, osmoles, and up to 20% of urea from "artificial urine" in slowly perfused dog ureter and bladder, and Walser et al (45) noted net loss of potassium, creatinine, and 7% of urea from urine perfusing ureters over 3 min duration in moderately dehydrated rats.…”

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confidence: 99%

Dietary protein affects urea transport across rat urothelia

Spector

Deng

Stewart

2012

American Journal of Physiology-Renal Physiology

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Spector DA, Deng J, Stewart KJ. Dietary protein affects urea transport across rat urothelia. Am J Physiol Renal Physiol 303: F944-F953, 2012. First published July 25, 2012 doi:10.1152/ajprenal.00238.2012.-Recent evidence suggests that regulated solute transport occurs across mammalian lower urinary tract epithelia (urothelia). To study the effects of dietary protein on net urothelial transport of urea, creatinine, and water, we used an in vivo rat bladder model designed to mimic physiological conditions. We placed groups of rats on 3-wk diets differing only by protein content (40,18,6, and 2%) and instilled 0.3 ml of collected urine in the isolated bladder of anesthetized rats. After 1 h dwell, retrieved urine volumes were unchanged, but mean urea nitrogen (UN) and creatinine concentrations fell 17 and 4%, respectively, indicating transurothelial urea and creatinine reabsorption. The fall in UN (but not creatinine) concentration was greatest in high protein (40%) rats, 584 mg/dl, and progressively less in rats receiving lower protein content: 18% diet, 224 mg/dl; 6% diet, 135 mg/dl; and 2% diet, 87 mg/dl. The quantity of urea reabsorbed was directly related to a urine factor, likely the concentration of urea in the instilled urine. In contrast, the percentage of instilled urea reabsorbed was greater in the two dietary groups receiving the lowest protein (26 and 23%) than in those receiving higher protein (11 and 9%), suggesting the possibility that a bladder/urothelial factor, also affected by dietary protein, may have altered bladder permeability. These findings demonstrate significant regulated urea transport across the urothelium, resulting in alteration of urine excreted by the kidneys, and add to the growing evidence that the lower urinary tract may play an unappreciated role in mammalian solute homeostasis.solute transport across bladder epithelia; urothelial creatinine transport; regulation of urothelial urea transport ALTHOUGH MAMMALIAN LOWER URINARY tract functions primarily as a short-term transit and storage vehicle for urine made by the kidneys (13), recent data demonstrate that mammalian urothelia (the epithelial cell lining of the urinary tract from renal pelvis to proximal urethra) is a surprisingly dynamic and complex tissue that may play an unappreciated role in water and solute homeostasis (35)(36)(37)(38)(39) reviewed in Ref. 22). While the urothelial permeability barriers, thought to reside in the apical membrane of the large "umbrella" cells lining the urinary tract lumens, the tight junction (TJ) between those cells, and the adherent overlying urinary glycosaminoglycans (GAG) layer (18,19,22,24,48), have been shown in vitro to have low permeability to water, urea, and ions (9,25,28), there are a number of physiological factors that might be expected to promote (even) passive diffusion of water and solutes across these barriers, including the large urinary tract lumenal surface area, long storage time of urine, enormous and changing concentration gradients for water, solutes, and ions, and ...

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Changes in composition of the urine in ureter and bladder at low urine flow

Cited by 99 publications

References 0 publications

The Expression of AQP1 and eNOS in Menopausal Rat Urinary Bladder

The Expression of AQP1 and eNOS in Menopausal Rat Urinary Bladder

The ROMK potassium channel is present in mammalian urinary tract epithelia and muscle

Dietary protein affects urea transport across rat urothelia

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