Intracellular sodium ion activity and sodium transport in rabbit urinary bladder.

Eaton, Douglas C.

doi:10.1113/jphysiol.1981.sp013804

Cited by 72 publications

(47 citation statements)

References 38 publications

(59 reference statements)

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“…Such a stoichiometry is not unusual and has been reported in other epithelia using radiotracer and electrical methodology (Nielsen, 1979;Zeuthen & Wright, 1981;Kirk, Halm & Dawson, 1980;Eaton, 1981;Hviid Larsen, Fuchs & Lindemann, 1979).…”

Section: Pump Stoichiometrymentioning

confidence: 84%

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Apical membrane permeability and kinetic properties of the sodium pump in rabbit urinary bladder.

Lewis¹,

Wills²

1983

The Journal of Physiology

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SUMMARY1. Previous studies have shown that aldosterone stimulates the rate of Na+ transport across the rabbit urinary bladder epithelium by increasing the apical membrane permeability to Na+. Paradoxically, ion-sensitive and conventional micro-electrode measurements demonstrated that intracellular Na+ activity aNa+ was essentially unchanged by aldosterone, i.e. aka+ was constant regardless of the rate of Na+ transport. The present study was designed to resolve this apparent contradiction.2. The effects of elevated, endogenous aldosterone levels produced by low-Na+ diet (Lewis & Diamond, 1976) on urinary bladder Na+ transport were investigated in vitro using Ussing-type chambers and intracellular conventional and ion-sensitive microelectrodes. Apical membrane selectivity and the kinetics of the Na+ pump were assessed as a function of hormone stimulation.3. The aldosterone-stimulated increase in Na+ transport was accounted for by increases in both the relative selective permeability of the apical membrane to Na+ and an increase in its absolute Na+ permeability.4. The kinetics of the Na+ pump were evaluated electrically by loading the cells with Na+ (monitored with Na+-sensitive micro-electrodes) or alternatively by manipulating serosal solution K+ concentration and measuring changes in the basolateral membrane electromotive forces and resistance. From these measurements the current generated by the pump was calculated as a function of intracellular Na+ or extracellular K+. The kinetics of the pump were not altered by aldosterone. A model of highly co-operative binding estimated Km for Na+ as 14-2 mm and 2-3 mm for K+. Hill coefficients for these ions were 2-8 and 1-8, respectively, consistent with a pump stoichiometry of 3 Na+ to 2 K+. The kinetic properties of the Na-K pump indicate that physiological levels of aka+ are poised at the foot of a step kinetic curve which energetically favours Na+ extrusion.

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Section: Pump Stoichiometrymentioning

confidence: 84%

“…The work of Eaton and co-workers (Eaton, 1981, Eaton, Frace & Silverthorn, 1982) indicates a 3:2 stoichiometry for the basolateral pump of the rabbit urinary bladder. We find this value is in good agreement with our electrical measurements.…”

Section: Pump Stoichiometrymentioning

confidence: 99%

Apical membrane permeability and kinetic properties of the sodium pump in rabbit urinary bladder.

Lewis¹,

Wills²

1983

The Journal of Physiology

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“…1,2 It has been suggested that the urothelium can mediate water and solute transport under certain circumstances. [3][4][5] Several studies have shown that the urinary bladder epithelium contains a sodium transporter 6 that has been identified as an epithelial sodium channel (ENaC), 7 which is known to be responsible for salt and fluid transport across the epithelia of many tissues. 8 Aquaporins (AQPs) are a family of intrinsic membrane proteins that function as water channels in many cell types involved in fluid transport.…”

Section: Introductionmentioning

confidence: 99%

Effect of detrusor overactivity on the expression of aquaporins and nitric oxide synthase in rat urinary bladder following bladder outlet obstruction

Kim

Choi

Song

et al. 2013

CUAJ

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E268research research AbstractBackground: Aquaporins (AQPs) have recently been reported to be expressed in rat and human urothelium. Nitric oxide (NO) is thought to play a role in the bladder overactivity related to bladder outlet obstruction (BOO). The purpose of this study is to investigate the effect of BOO on the expression of AQP2-3 and nitric oxide synthase (NOS) isoforms in rat urothelium. Methods: Female Sprague-Dawley rats (230-240 g, n = 60) were divided into 2 groups. The control group (n = 30) and the partial bladder outlet obstruction (BOO) group (n = 30). After 4 weeks, we performed a urodynamic study to measure the contraction interval and contraction pressure. The expression and cellular localization of AQP2-3, endothelial nitric oxide synthase (eNOS) and neuronal nitric oxide synthase (nNOS) were determined by Western blot and immunohistochemistry. Results: On the cystometrogram, the estimated contraction interval time (minutes, mean ± SE) was significantly lower in the BOO group (3.0 ± 0.9) than in the control group (6.3 ± 0.4; p < 0.05). AQP2 was localized in the cytoplasm of the epithelium, whereas AQP3 was found only in the cell membrane of the epithelium. The protein expression of AQP2-3, eNOS and nNOS was significantly increased in the BOO group. Conclusion: Detrusor overactivity induced by BOO causes a significant increase in the expression of AQP2-3, eNOS, and nNOS in rat urinary bladder. This may imply that the AQPs and NOS isoforms have a functional role in the bladder dysfunction that occurs in association with BOO.

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“…Indeed, significant net transport (both lumen to blood and blood to lumen) of solutes, including urea, creatinine, sodium, potassium, and chloride, usually down their respective blood/urine gradients, has been demonstrated in vivo in rabbits and rats and studies of perfused dog ureter (14,29) and bladder (8,9,14,21,27). Furthermore, a number of studies have shown that rabbit and guinea pig urinary bladder epithelium contain an aldosterone-stimulated, amiloride-inhibited sodium transporter (2,16), which has recently been identified by Northern blot analysis as the epithelial sodium channel (22). The epithelial sodium channel is known to be responsible for salt and fluid transport across epithelia of many tissues (6).…”

mentioning

confidence: 99%

Expression, localization, and regulation of aquaporin-1 to -3 in rat urothelia

Spector

Wade²,

Dillow

et al. 2002

American Journal of Physiology-Renal Physiology

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. Expression, localization, and regulation of aquaporin-1 to -3 in rat urothelia. Am J Physiol Renal Physiol 282: F1034-F1042, 2002. First published January 29, 2002 10.1152/ajprenal.00136.2001.-Although mammalian urothelia are generally considered impermeable to constituents of urine, in vivo studies in several species indicate urothelial transport of water and solutes under certain conditions. This study investigates the expression, localization, and regulation of aquaporin (AQP)-1, -2, and -3 in ureteral and bladder tissues in 48-h dehydrated and water-loaded female Wistar rats. Immunoblots of homogenates of whole ureter and bladder identified characteristic ϳ28-and 35-to 44-kDa bands for AQP-1, -2, and -3. AQP-1 was localized to capillary and arteriole endothelial cells, whereas AQP-2 and -3 circumferentially lined the epithelial cell membranes except for the apical membrane of the epithelial cells adjacent to the lumens of both ureter and bladder. AQP-2 was also present in epithelial cell cytoplasm. Dehydration resulted in 160-200% increases of AQP-3 signal and 24-49% increases of AQP-2 signal but no change in AQP-1 signal on immunoblots of homogenates of ureters and bladders. AQPs in genitourinary tract urothelia likely play a role in the regulation of epithelial cell volume and osmolality and may play a role in bulk water movement across urothelia.Western blot analysis; immunocytochemistry; water transport IT IS GENERALLY ASSUMED THAT the mammalian lower urinary tract is an impermeable transit and storage system and that micturated urine is identical to that excreted by kidneys (7). In fact, recent in vitro studies have documented very low urothelial permeability to water, ions, and nonelectrolytes and demonstrated that a major permeability barrier resides in the apical luminal membrane of the epithelial cells ("umbrella cells") lining the bladder lumen (reviewed in Ref. 15;19).Although urothelial permeability to water and solutes may be low, it is finite, and the possibility that urine might be significantly modified in transit by the lower urinary tract is plausible given the large urothelial surface area and long elapsed time between egress of urine from collecting ducts and micturation. Indeed, significant net transport (both lumen to blood and blood to lumen) of solutes, including urea, creatinine, sodium, potassium, and chloride, usually down their respective blood/urine gradients, has been demonstrated in vivo in rabbits and rats and studies of perfused dog ureter (14, 29) and bladder (8,9,14,21,27). Furthermore, a number of studies have shown that rabbit and guinea pig urinary bladder epithelium contain an aldosterone-stimulated, amiloride-inhibited sodium transporter (2, 16), which has recently been identified by Northern blot analysis as the epithelial sodium channel (22). The epithelial sodium channel is known to be responsible for salt and fluid transport across epithelia of many tissues (6).Although isotopic movement of D 2 O or isotopically labeled water across mammalian urothelia has bee...

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Intracellular sodium ion activity and sodium transport in rabbit urinary bladder.

Cited by 72 publications

References 38 publications

Apical membrane permeability and kinetic properties of the sodium pump in rabbit urinary bladder.

Apical membrane permeability and kinetic properties of the sodium pump in rabbit urinary bladder.

Effect of detrusor overactivity on the expression of aquaporins and nitric oxide synthase in rat urinary bladder following bladder outlet obstruction

Expression, localization, and regulation of aquaporin-1 to -3 in rat urothelia

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