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At least 145 records · Page 8Linked to original sources
PubMed1987

Band 3 is the basolateral anion exchanger of dark epithelial cells of turtle urinary bladder.

The turtle urinary bladder serves as a model for collecting duct functions in the mammalian kidney. The epithelium of both the turtle bladder and the mammalian collecting duct can generate a steep gradient for H+ ions between blood and urine. Secretion of H+ into the urine is coupled to a basolateral efflux of HCO-3 that appears to be exchanged mainly against Cl-. Here we show that approximately 80% of the dark cells of the bladder contain a 110,000 relative molecular weight (Mr) analogue of the turtle erythrocyte anion exchanger, band 3. The band 3 analogue is confined to the basolateral cell surface and is absent from the apical membrane. A minor population of the dark cells (approximately 20%), which have been previously suggested to represent reverse cells that are involved in HCO-3 secretion rather than absorption, appears not to express a band 3-like anion exchanger, at either the apical or the basolateral membrane. The bladder band 3 protein is colocalized with actin and isoforms of ankyrin (200,000 Mr) and spectrin (230,000 Mr) along the basolateral membrane. Linkage of band 3 via ankyrin to the spectrin-actin lattice may restrict this anion exchanger to the basolateral membrane surface. In view of our previous observation of a band 3-like anion exchanger in the collecting duct epithelium of the rat kidney, these findings point to a common molecular basis for acid-base transport in the mammalian collecting duct and the reptilian urinary bladder.

Animals↗
PubMed1987

Vasoactive intestinal peptide stimulates alkali excretion in turtle urinary bladder.

The turtle urinary bladder possesses an active transport mechanism for the electrogenic secretion of alkali. This process is independent of exogenous Cl and Na, induced by cyclic AMP (cAMP), and potentiated in bladders from NaHCO3-loaded (alkalotic) turtles. In the present study, it is shown that the serosal addition of vasoactive intestinal peptide (VIP) induces rapidly developing parallel increases in alkali secretion and in the short-circuiting current carried by this secretion. The VIP-induced increment in alkali secretion is greater in the presence than in the absence of an exogenously added phosphodiesterase inhibitor. Additions of a cAMP analog subsequent to the VIP-induced alkali secretion fail to induce any further increase in alkalinization. These results provide evidence for the action of VIP as a hormonal up regulator of alkali excretion in the turtle urinary bladder.

1-Methyl-3-isobutylxanthine↗
PubMed1991

Identification of a stretch-activated monovalent cation channel from teleost urinary bladder cells.

The urinary bladder of euryhaline teleost is an important osmoregulatory organ which absorbs Na+, Cl-, and water from urine. Using patch clamp technique, single stretch-activated channels, which were permeable to K+ and Na+ (PNa/PK approximately 0.75) and had conductances of 55 and 116 pS, were studied. In excised, inside-out patches which were voltage-clamped in the physiological range of membrane potential, the single-channel open probability (Po) was low (approximately 0.02), and increased to a maximum of 0.9 with applied pipette suction. Single-channel conductance also increased with suction. The channels showed adaptation to applied suction and relaxed to a steady-state activity about 20 seconds after application of suction. The Po increased up to 0.9 with strong membrane depolarization (Vm = 0 to +80 mV); however, there was little dependence of Po on membrane potential in the physiological range. The kinetic data suggest that there is one conducting state and at least two non-conducting states of the channel. The open-time constant increased with suction but remained unchanged with membrane potential (Vm = -70 to +60 mV). The mean closed-time of the channel decreased with suction and membrane depolarization. These results demonstrate the presence of a non-selective monovalent cation channel which may be involved in cell volume regulation in the goby urinary bladder. Additionally, this channel may function as an enhancer of Na+ influx and K+ efflux across the bladder cell as part of transepithelial ion transport if it is located in apical membrane.

Animals↗
PubMed2000

Possible role of endothelin-1 in the rabbit urinary bladder hyperplasia secondary to partial bladder outlet obstruction.

OBJECTIVES: Urinary bladder hypertrophy and hyperplasia are common features of bladder outlet obstruction (BOO). The urinary bladder is known to synthesize endothelin-1 (ET-1), which is a potent vasoconstrictor peptide with mitogenic properties. Using an animal model of partial BOO, we investigated the potential role of ET-1 and its receptor subtypes (ET(A) and ET(B)) in bladder smooth muscle cell (SMC) proliferation. MATERIALS AND METHODS: Partial BOO was produced in adult male New Zealand White rabbits. After 3 weeks, the bladder was removed and SMCs from the dome and bladder neck were grown using standard explant methodology. At passage 2, the cells were made quiescent and then further incubated in foetal calf serum (FCS), control age-matched rabbit serum (CRS) or partial BOO serum (BRS) in the presence or absence of ET(A)-antagonist (BQ123) or ET(B)-antagonist (BQ788). SMC proliferation was then measured 24 h later with 5-bromo-2'deoxy-uracil and by cell counting using a haemocytometer at 48 h. Immunostaining for alpha-actin was performed on detrusor and bladder neck cells to confirm the presence of smooth muscle cells. RESULTS: BQ123 and BQ788 did not influence detrusor or bladder neck SMC proliferation in FCS or CRS. However, in the presence of BRS, BQ123 and BQ788 (100 nmol/L) significantly (p = 0.008) inhibited detrusor and bladder neck SMC proliferation. Cell counts were significantly reduced from the detrusor (p = 0.03, p = 0.01 with BQ123 and BQ788, respectively) and bladder neck (p = 0.01 for both BQ123 and BQ78). CONCLUSIONS: These results suggest that ET antagonists may have a role in preventing SMC hyperplasia associated with partial BOO.

Animals↗
PubMed2005

Use of abdominal wall with mesothelium as a substrate for reconstitution of urinary bladder wall: replacement of the mesothelium by the urothelium and complete bladder wall reconstruction.

OBJECTIVE: The urinary bladder has considerable regenerative ability and may enable reconstitution of the urinary bladder if used appropriately. MATERIAL AND METHODS: Rat urinary bladders were allotransplanted onto the inner surface of the abdominal wall with the urothelium facing the mesothelial cells. The ureters, urethra and blood supply were left intact. RESULTS: A week after the operation, the mesothelium of the abdominal wall was replaced by the urothelium from the donor urinary bladder and a cyst was formed, the inner surfaces of which were completely covered with the urothelium. After a few months, the submucosal tissue and muscular layer had also moved to cover the wall, forming an almost complete urinary bladder. The mucosal membrane formed complex folds, which was probably due to overgrowth of the epithelial cells and the submucosal connective tissues. The area derived from the abdominal wall showed only minimal shrinkage, whereas the abdominal wall from which the mesothelium had been removed showed significant shrinkage. CONCLUSION: This method is potentially useful for the reconstruction of urinary bladders.

Abdominal Wall↗
PubMed1987

Radical cystectomy and ileocaecal bladder reconstruction for carcinoma of the urinary bladder. A study of 130 patients.

One hundred and thirty patients underwent radical cystectomy and ileocaecal bladder reconstruction for carcinoma of the urinary bladder. The actuarial 5-year survival rate was 45%. Local pelvic recurrence was noted in 26.3% of patients. Most of those in the series (81.9%) had perfect control of micturition. Intravenous urography performed up to 10 years post-operatively showed preservation of renal configuration in 92.2%. The normal flow curves recorded showed that it was possible to achieve a balanced vesicourethral unit. Ileocaecal bladder reconstruction is less disabling than urinary diversion after radical cystectomy.

Adult↗
PubMed1996

Immunohistochemically demonstrated variation in expression of cathepsin E between uracil-induced papillomatosis and N-butyl-N-(4-hydroxybutyl)nitrosamine-induced preneoplastic and neoplastic changes in rat urinary bladder.

Expression of rat urinary bladder cathepsin E in benign papillomatosis induced by uracil and various stages of N-butyl-N-(4-hydroxybutyl)nitrosamine (BBN)-induced carcinogenesis was investigated immunohistochemically. Seven-week-old, male F344/DuCrj rats were used. In the normal urothelium of control rats, cathepsin E stained in all layers of cells, although in umbrella cells and some basal cells the reaction was relatively weak. In rats given a diet containing 3% uracil for 5 weeks immunoreactivity of cathepsin E in uracil-induced papillomatosis was consistently homogeneous in all layers, but weaker than in normal urothelium. In rats given 0.05% BBN in drinking water for 12 weeks and subsequently maintained without treatment for 48 weeks cells with little cathepsin E, never observed in normal urothelium, appeared at 5 weeks above the basement membrane in the earliest stage of BBN-induced urinary bladder cancer (simple hyperplasia). Throughout the neoplastic process, groups of cells with a little cathepsin E were randomly distributed, with expression in the urothelium being markedly unstable. Almost all areas of squamous cell proliferation in TCC were negative for cathepsin E. Instability of cathepsin E expression in rat urothelium therefore appears characteristic for carcinogenesis and offers the possibility of using this feature as an early biomarker for urinary bladder carcinogenesis.

Animals↗
PubMed2002

2-Aminoethoxydiphenyl borate causes dissociation between membrane electrical and mechanical activity in guinea-pig urinary bladder smooth muscle.

Physiological functions of urinary bladder profoundly reflect smooth muscle mechanical activity. Urinary bladder smooth muscle itself produces myogenic rhythmic contraction, and this spontaneous mechanical event could be the fundamental determinant of urinary bladder functions. The spontaneous contraction of urinary bladder smooth muscle is thought to be triggered primarily by the action potential generated in this smooth muscle cell. Modulators of ion channels contributing to the configuration of action potential also affect urinary bladder smooth muscle mechanical activity as expected exactly from the effects on the electrical event. In the present study, we show that the frequency of action potential recorded in intact strip of guinea-pig urinary bladder smooth muscle is dramatically increased by 2-aminoethoxydiphenyl borate (2-APB; 30 microM) from 0.2 Hz to 1 Hz (approximately 500% increments). In contrast to an increasing effect expected from the membrane electrical alterations, mechanical activity (both contraction amplitude and frequency) of this smooth muscle is unexpectedly reduced by the same concentration of 2-APB to approximately 35% of the control. The present results firstly show an apparent dissociation of electrical-mechanical coupling in urinary bladder smooth muscle. The alteration of membrane electrical activity might not be the exclusive trigger mechanism responsible for the generation of spontaneous rhythmic contraction of this smooth muscle.

Action Potentials↗
PubMed1999

Bladder afferent pathway and spinal cord injury: possible mechanisms inducing hyperreflexia of the urinary bladder.

Lower urinary tract dysfunction is a common problem in patients with spinal cord injury (SCI). Since the coordination of the urinary bladder and urethra is controlled by the complex mechanisms in spinal and supraspinal neural pathways, SCI rostral to the lumbosacral level disrupts voluntary and supraspinal control of voiding and induces a considerable reorganization of the micturition reflex pathway. Following SCI, the urinary bladder is initially areflexic. but then becomes hyperreflexic because of the emergence of a spinal micturition reflex pathway. Recent electrophysiologic and histologic studies in rats have revealed that chronic SCI induces various phenotypic changes in bladder afferent neurons such as: (1) somal hypertrophy along with increased expression of neurofilament protein; and (2) increased excitability due to the plasticity of Na+ and K+ ion channels. These results have now provided detailed information to support the previous notion that capsaicin-sensitive, unmyelinated C-fiber afferents innervating the urinary bladder change their properties after SCI and are responsible for inducing bladder hyperreflexia in both humans and animals. It is also suggested that the changes in bladder reflex pathways following SCI are influenced by neural-target organ interactions probably mediated by neurotrophic signals originating in the hypertrophied bladder. Thus, increased knowledge of the plasticity in bladder afferent pathways may help to explain the pathogenesis of lower urinary tract dysfunctions after SCI and may provide valuable insights into new therapeutic strategies for urinary symptoms in spinal cord-injured patients.

Afferent Pathways↗
PubMed2006

[Rare cases of acute urineous peritonitis as a consequence of a spontaneous rupture of the urinary bladder].

Perforation of the urinary bladder is, in most cases, caused by a blunt or penetrative trauma, respectively by an iatrogenic trauma. A spontaneous rupture of the urinary bladder is very rare. In the literature, its relation with alcohol abuse is speculated. Due to their minimal frequency rates, the diagnosis is very difficult and, not uncommonly, the diagosis is verified only upon surgical revision. The authors present two cases of urgent diffuse peritonitis originating from spontaneous perforations of the urinary bladder.

Acute Disease↗