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PubMed1991

Functional expression of urea channels in amphibian oocytes injected with frog urinary bladder mRNA.

In amphibian urinary bladder epithelium, vasopressin increases passive urea permeability, concomitant with the appearance of a facilitated urea transport. Amphibian oocytes from Xenopus laevis and Rana esculenta were microinjected with total or fractionated poly(A+) RNA isolated from frog urinary bladder epithelial cells. After several (3-5) days at 18 degrees C, the urea flux was assayed by measuring the uptake and efflux of [14C]urea in water-injected and mRNA-injected oocytes. A 2 to 3-fold increase of urea transport was detected in oocytes injected either with total mRNA or with a 6-10 kilobase mRNA fraction, when compared with water-injected oocytes. This expression of urea channels was inhibited by 0.1 mM phloretin (50% inhibition) and 0.1 mM nitrophenylthiourea (up to 70% inhibition). On the contrary, no expression was detected in brain mRNA-injected oocytes. These results show the specific functional expression of the phloretin- and NPTU-sensitive urea channel (or carrier) from frog urinary bladder epithelial cells, providing an approach for the expression cloning of these urea channels.

Animals↗
PubMed1985

Organization of sympathetic responses to distension of urinary bladder.

Distension of the urinary bladder can cause reflex pressor responses, which appear to be mediated by increased sympathetic activity. However, preganglionic upper thoracic sympathetic activity is excited inconsistently by bladder distension in intact and spinal animals. The objective of this investigation was to determine if any of the postganglionic nerves originating from thoracic and lumbar spinal segments are consistently excited by vesical afferent nerves. Responses of external carotid, renal, and splenic sympathetic nerves to distension of the urinary bladder were evaluated in chloralose-anesthetized cats. In addition, the potential preferential spinal segmental distribution of vesico-sympathetic reflexes was assessed by comparing the magnitudes of external carotid, renal, and splenic nerve responses. Distension of the urinary bladder with 5-35 ml saline initiated vesical contractions to pressures of 45-90 cmH2O and caused inconsistent changes in arterial pressure and activity of renal and splenic sympathetic nerves. External carotid nerves were excited by this stimulus. Vesical distension with 12-50 ml saline caused contractions to vesical pressures of 135-175 cmH2O and produced consistent increases in arterial pressure and activity of all three nerves. Thus activation of vesical afferent nerves by high pressure produced excitation of upper thoracic vasomotor neurons and of two major components of splanchnic and lumbar sympathetic outflow. The magnitudes of external carotid, renal, and splenic sympathetic responses were not different, illustrating that propriospinal circuits thought to mediate vesicosympathetic responses are not organized segmentally.

Afferent Pathways↗
PubMed1992

Effects of acute in vitro overdistension of the rabbit urinary bladder on DNA synthesis.

Urinary bladder outflow obstruction induces a myriad of structural and functional changes in the organ. Among the morphological responses to outlet obstruction is both hyperplasia and hypertrophy of specific cellular elements. The initial event which has been implicated in the initiation of the response to outflow obstruction is an initial period of high intravesical pressure and subsequent distention of the bladder. In a previous study, it was shown that at one day following partial outlet obstruction there was a marked increase in thymidine labelling of the urothelium, at 3-5 days, the labeling shifted from the urothelium to the interstitial and serosal elements. The current study was designed to determine if acute distention of the urinary bladder can induce an increase in DNA synthesis (3H-thymidine incorporation), and localize the increased DNA synthesis via autoradiography of 3H-thymidine. In this study, the bladders of adult male New Zealand white rabbits were mounted in isolated in vitro baths. Each control bladder was filled to either 5 or 20 ml. with saline, or distended to 120% of capacity. The bladders were incubated for 7 hours at which time 3H-thymidine was placed both within and outside the bladder for an additional one hour. At the end of the time the bladder was divided at the ureteral orifices into bladder body and base, and each body and base divided into two sections. One section of bladder body and base was quantitatively analyzed for both labelled and unlabelled DNA; the second section was fixed and prepared for autoradiography. The results can be summarized as follows: 1) Acute overdistention for 8 hours induced a slight decrease in the DNA concentration which was mediated by edema of the bladder wall. 2) Acute overdistention induced a 5-fold increase in 3H-thymidine incorporation in the bladder body and a 3-fold increase in the bladder base. Radioautoradiography of the overdistended bladders showed significant and substantial labelling which was confined to the urothelial basal cells. The control bladders showed little or no labelling. These results are consistent with the theory that acute distention following partial outlet obstruction initiates the proliferative response of the bladder to outlet obstruction, and the urothelium is the initial target of the proliferative response. Functionally, the proliferative response may serve to maintain the structural as well as functional integrity of the bladder.

Animals↗
PubMed1999

An extended-release formulation of oxybutynin chloride for the treatment of overactive urinary bladder.

Detrusor instability, or urinary incontinence, is common in elderly patients, particularly elderly women. The clinical symptoms of overactive, or unstable, urinary bladder include urge urinary incontinence, urgency, and frequency. Mixed urinary incontinence, which comprises urge urinary incontinence and stress incontinence, is manifested by increased intraabdominal pressure on coughing or sneezing. The detrusor muscle of the bladder is under the control of the parasympathetic, or muscarinic, nervous system. The drug of choice in this condition is oxybutynin chloride, which has the ability to block acetylcholine released from parasympathetic nerves in the urinary bladder, preventing contractions of the muscle and exerting a direct spasmolytic effect on the bladder. A new extended-release oral tablet formulation, OROS oxybutynin, uses osmotic pressure to deliver the drug at a controlled rate over approximately 24 hours. It resembles a conventional tablet but has a two-part core consisting of a drug layer and below it, a "push" layer containing osmotically active components, the whole surrounded by a semipermeable membrane with a laser-drilled opening in the drug side. Water in the gastrointestinal tract enters the tablet and mixes with the drug to form a suspension. The "push" layer expands and pushes the suspended drug out of the orifice and into the gastrointestinal tract for eventual absorption. Pharmacokinetic studies have indicated a slow rise in mean plasma concentration of the isomer R-oxybutynin for 4 to 6 hours after a single dose of OROS oxybutynin, followed by maintenance of steady concentrations for up to 24 hours, minimizing the fluctuations between peak and trough associated with TID dosing of 5-mg immediate-release oxybutynin tablets. Efficacy and safety studies comparing the extended-release with the immediate-release formulation of oxybutynin demonstrated equivalent efficacy in patients with overactive urinary bladder. The adverse-event profile of oxybutynin is similar to that of a typical anticholinergic agent such as atropine--dry mouth, constipation, somnolence, blurred vision, headache, and gastrointestinal pain--although in 2 clinical studies, the incidence of dry mouth was less with the extended-release formulation. Once-daily dosing with OROS oxybutynin appears to be well tolerated and effective, as well as convenient, for the treatment of overactive bladder, particularly for elderly patients using multiple medications.

Cholinergic Antagonists↗
PubMed1983

The effect of arylazido aminopropionyl ATP on atropine resistant contractions of the cat urinary bladder.

This work was designed to study neurogenic, atropine resistant contractions of the cat urinary bladder. Urinary bladder contractions were induced by pelvic nerve stimulation (PNS) and the administration of acetylcholine (Ach) and purine compounds. The results show that atropine (2 mg/kg) depresses the maintained portion (phase 2) of PNS-induced contractions and Ach-induced contractions while having no effect on the initial portion (phase 1) of the PNS-induced contractions or those contractions induced by the purines. Arylazido aminopropionyl ATP (ANAPP3), an ATP antagonist, depressed phase 1 of the PNS contraction and the purine induced contractions. These results suggest that ATP is responsible for at least part of the atropine-resistant contractions of the cat urinary bladder.

Acetylcholine↗
PubMed1996

Sympathoadrenal activity in the visceral (viscerovascular) reflexes to distension of the urinary bladder.

Distension of the urinary bladder can cause reflex pressor responses, which appear to be mediated by increased sympathetic activity. We correlated the involvement of the adrenal gland (medulla) itself and adrenosympathetic nerve activities with the viscerovascular reflexes and their role in controlling the reflex response following distension of the urinary bladder. The experiments were performed in 37 chloralose anesthetized cats. It was observed that reflex rise of blood pressure was not affected by intravenous administration of propranolol, indicating that the beta-adrenoceptors (inhibitory effect) were not involved in such reflex. Phentolamine, hexamethonium and guanethidine sulfate completely prevented the reflex action, and comparison of the magnitudes of responses and this inhibitory effect suggests the participation of alpha-adrenoceptors (excitatory effect) as a result of the vasoconstriction that develops during bladder distension. In the present study, we determined that adrenalectomy significantly (p < 0.0001) altered the magnitudes of reflex response during bladder distension. The 10.4% (systolic, p < 0.001) and 10.6% (diastolic, p < 0.01) change in reflex response was mediated directly through adrenomedullary catecholamines, and the 14.8% (systolic, p < 0.001) and 23.8% (diastolic, p < 0.0001) change in vasopressor response was mediated by adrenosympathetic ganglionic activity. The single unit activity from the central cut end of the adrenal sympathetic nerve was recorded for direct evidence. An increase in electrical activity (1-3 to 7-10 spikes/s; p < 0.001) of the adrenal sympathetic nerve with the rise of blood pressure during bladder distension was observed. We concluded that, like other sympathetic nerves, the adrenal sympathetic nerve contributed to the enhancement of blood pressure during bladder distension. This result also explains the partial inhibition of reflex hypertension during bladder distension after adrenalectomy. These studies also conclude that the adrenal gland and adrenosympathetic nerve act as facilitatory modulators in maintaining catecholamine secretion under conditions of stress (urinary bladder distension).

Animals↗
PubMedDate not supplied

[Intestinal metaplasia of mucosal epithelium of the urinary bladder].

4 cases of urinary bladder intestinal metaplasia are reported. One adenoma and one adenocarcinoma of intestinal type were discovered. Immunohistochemically, expression of meconial intestinal antigen beta 1 MA in the cytoplasm and on the apical surface of goblet-like cells was observed.

Aged↗
PubMed1984

Ion and water transport by the flounder urinary bladder: salinity dependence.

Urinary bladders from seawater-acclimated (SW) flounder had a transepithelial resistance (Rt) of congruent to 2,000 omega X cm2 and absorbed Na and Cl at equal rates of about 3 mueq X cm-2 X h-1 in an electrically silent manner; the short-circuit current (Isc) was 0.03 +/- 0.01 mueq X cm-2 X h-1. The transport of Na and Cl was only partially coupled. Removal of Na (or Cl) from the bathing solutions reduced net Cl (or Na) absorption by only 60%, yet there was neither a change in transepithelial potential nor the appearance of a short-circuit current that could be associated with the net Cl (or Na) transport that remained. Bladders from freshwater-acclimated (FW) flounder had a fivefold lower Rt and exhibited the same partially coupled and equal Na and Cl transport, but the ion transport rates were twice as large as those of SW bladders and the bladders exhibited a significant Isc of 0.51 +/- 0.08 mueq X cm-2 X h-1. The rate of fluid transport was much lower in FW than in SW bladders, reflecting a sixfold decrease in hydraulic conductivity (Lp). In both SW and FW bladders a large portion of the serosal-to-mucosal ion movement appears to be through nonconductive pathways.

Animals↗
PubMed2001

Regional variation in myosin isoforms and phosphorylation at the resting tone in urinary bladder smooth muscle.

Urinary bladder filling and emptying requires coordinated control of bladder body and urethral smooth muscles. Bladder dome, midbladder, base, and urethra showed significant differences in the percentage of 20-kDa myosin light chain (LC20) phosphorylation (35.45 +/- 4.6, 24.7 +/- 2.2, 13.6+/- 2.1, and 12.8 +/- 2.7%, respectively) in resting muscle. Agonist-mediated force was associated with a rise in LC20 phosphorylation, but the extent of phosphorylation at all levels of force was less for urethral than for bladder body smooth muscle. RT-PCR and quantitative competitive RT-PCR analyses of total RNA from bladder body and urethral smooth muscles revealed only a slight difference in myosin heavy chain mRNA copy number per total RNA, whereas mRNA copy numbers for NH2-terminal isoforms SM-B (inserted) and SM-A (noninserted) in these muscles showed a significant difference (2.28 x 10(8) vs. 1.68 x 10(8) for SM-B and 0.12 x 10(8) vs. 0.42 x 10(8) for SM-A, respectively), which was also evident at the protein level. The ratio of COOH-terminal isoforms SM2:SM1 in the urethra was moderately but significantly lower than that in other regions of the bladder body. A high degree of LC20 phosphorylation and SM-B in the bladder body may help to facilitate fast cross-bridge cycling and force generation required for rapid emptying, whereas a lower level of LC20 phosphorylation and the presence of a higher amount of SM-A in urethral smooth muscle may help to maintain the high basal tone of urethra, required for urinary continence.

Animals↗
PubMed1996

Two mathematical models explain the variation in cystometrograms of obstructed urinary bladders.

Overdistension of the urinary bladder, secondary to outlet obstruction, causes cellular changes in the bladder wall, including hypertrophy of the smooth muscle cells, which increase bladder mass. To investigate the effects of increased mass on the cystometrogram (CMG), we have developed two mathematical models. In the first model, we assume that mass is added such that the largest bladder volume at zero transmural pressure, the zero pressure volume (ZPV), is constant, It predicts increased pressures and decreased compliance in the CMG. In the second model, we assume that both mass and ZPV increase proportionally. It predicts unchanged pressures, increased compliance, and increased capacity in the CMG. These results allow use to divide animal experiments in the literature into two groups. Cystometrograms performed on animals that have had outlet obstruction induced by a cuff method, inducing a small increase in mass, belong to the first group: hypertrophy with no change in ZPV. Cystometrograms performed on animals that have had outlet obstruction induced by a ligature method, inducing a large increase in mass, belong to the second group: hypertrophy with increased ZPV. We conclude that increased ZPV results from a more severe obstruction which is indicated by the increased capacity and compliance.

Animals↗
PubMed1995

Microvasculature of the rabbit urinary bladder.

BACKGROUND: The urinary bladder requires a rich blood supply to maintain its functions, the storage and release of urine. Specialized properties of the bladder vasculature might be anticipated to ensure the integrity of this blood supply, because it is known that blood flow is reduced by distension during bladder filling. However, the bladder vasculature has been described in detail only at the gross level. A comprehensive, three-dimensional view of the blood supply to the bladder wall is presented here. METHODS: The microvasculature of the bladder of male New Zealand white rabbits was described using the combination of vascular corrosion casting, alkali digestion, light microscopy, and scanning and transmission electron microscopy. Following administration of an anticoagulant and an overdose of anesthetic, the abdominal aorta was cannulated just above the inferior mesenteric artery to permit flushing of the distal vasculature. The bladder vasculature was cleared of blood with buffered saline and then either perfuse-fixed with buffered 2% glutaraldehyde and sectioned, or filled with "Mercox" resin to prepare vascular corrosion casts. Casts were cleaned with NaOH, formic acid, and water. In some cases fixed bladders were partially digested with NaOH to expose the mucosal capillary plexus. RESULTS: The bladder is supplied with blood by single, left and right vesicular branches of the internal or external iliac arteries. The serpentine vesicular arteries extend along the lateral borders of the bladder from base to apex just deep to the serosal surface and send dorsal and ventral branches to supply the dorsal and ventral bladder walls. Veins accompany the arteries and exhibit numerous valves. A very dense complex of vessels at the apex of the bladder apparently serves to accommodate bladder distension. The muscularis and submucosa contains few vessels, but the mucosa is well vascularized. An especially dense capillary plexus is present in the lamina propria at its junction with the transitional epithelium. In the relaxed bladder these capillaries lie in grooves formed by the basal layers of the epithelium. The endothelial cells of these capillaries display few cytoplasmic vesicles and are continuous or fenestrated. These capillaries are often invested with pericytes. The mucosal capillary plexus may be associated with an epithelial transport function or may be necessary for urothelial metabolism or maintenance of the barrier function of the urothelium. Unusual capillary tufts, possibly associated with vascular lymphatic tissue, are found associated with the main vessels on the lateral walls in the basal half of the bladder. CONCLUSIONS: These methods present a clear, comprehensive, three-dimensional view of the microvasculature of the bladder wall. They also identify several unique features of this vasculature and provide a basis for studies of the response of this vasculature to pathologic states and experimental manipulation.

Animals↗
PubMed2001

Molecular cytogenetic alterations associated with rapid tumor cell proliferation in advanced urinary bladder cancer.

Invasive urinary bladder carcinomas are characterized by a high number of cytogenetic alterations which are thought to pinpoint the location of critical genes, some of which may be involved in cell cycle control. To identify genomic alterations that may affect such genes the proliferative activity (Ki67 labeling index) was assessed in 93 invasively growing bladder carcinomas analyzed by comparative genomic hybridization. Only a few changes were significantly associated with rapid tumor cell proliferation, including 3p+ (p=0.0357), 6p+ (p=0.003), 8q+ (p=0.0273), and 11q- (p=0.0329). Among these alterations 6p+ is of particular interest because high level 6p22 amplifications occur frequently in bladder cancer. The particular strong association between 6p+ and a high tumor cell proliferation being independent of grade and stage suggests that a putative oncogene on 6p22 involved in cell cycle regulation.

Carcinoma, Transitional Cell↗
PubMed1980

Compensatory increase of responses to nerve stimulation of the partially denervated rat urinary bladder.

The rat urinary bladder was deprived of half of its innervation by removing the pelvic ganglion on one side. The motor response of such a partially denervated bladder to stimulation of the pelvic nerve on the other side were examined 1 week, 1 month and 2 months postoperatively. On all three occasions the increase in pressure of the operated bladder was larger than that of the control bladder; the enlargement was most marked 2 months after operation. The responses were further enlarged by eserine, and markedly reduced by atropine. The present results combined with those of previous investigations, showing a rapid recovery in the activity of the acetylcholine forming enzyme from a reduced level and a transient supersensitivity to chemical stimuli after unilateral removal of the pelvic ganglion, suggest that the enlarged responses to nerve stimulation 1 week postoperatively are mainly due to sensitization, while those observed at the later stages are due to collateral sprouting from the cholinergic nerve fibres of the intact pelvic nerve.

Adrenergic Fibers↗
PubMed1976

Alterations in membrane-associated particle distribution during antidiuretic challenge in frog urinary bladder epithelium.

Frog urinary bladder epithelium has been examined by freeze-fracture electron microscopy of preparations previously fixed by glutaraldehyde either at rest or during antidiuretic challenge. All the agonists tested were observed to induce membrane particle clustering in the A face of the apical plasma membrane of granular cells. This was the case for the natural hormone (hypophysical extracts) and its presumed cellular mediator, adenosine 3',5'-monophosphate. Particle clustering was observed both in the presence and in the absence of water net flow and is thus independent of these movements. Clusters were also observed during hydrosmotic challenge by hypertonic serosal media, a condition which depresses transepithelial sodium transport. No complementary patterns of these A face clusters could be found on the B face. The significance of these membrane-associated particle clusters is discussed in terms of membrane structure and function.

Animals↗
PubMed1993

Severity of promotion by sodium salts of succinic acid in rat urinary bladder carcinogenesis correlates with sodium ion concentration under conditions of equal urinary pH.

Elevation of urinary pH and Na ion concentration induced by feeding high doses of sodium salts plays a crucial role in promotion of urinary bladder carcinogenesis in male rats initially treated with N-butyl-N-(4-hydroxybutyl)nitrosamine (BBN). In the present study, urinary bladder carcinogenesis in male F344 rats was promoted by feeding the mono- and di-sodium salts of succinic acid, and the activity was enhanced by varying urinary sodium ion concentration under conditions of equally high pH. In Experiment 1, the rats were given 0.05% BBN in their drinking water for 4 weeks and then fed basal diet containing 5% succinic acid, 5% sodium succinate (Na-Suc) or 5% di-sodium succinate (2Na-Suc) for 32 weeks. The development of carcinomas in the urinary bladder was enhanced by treatment with Na-Suc and with 2Na-Suc. 2Na-Suc induced larger urinary bladder tumors than the Na-Suc. In Experiment 2, 5% Na-Suc and/or 5% 2Na-Suc were fed to the rats for 8 weeks without prior BBN treatment. Induction of simple hyperplasia as observed by light microscopy, was greater in rats fed 2Na-Suc than Na-Suc. Increased 5-bromo-2'-deoxyuridine labeling index and alterations of the urothelial surface observed by scanning electron microscopy of the urinary bladder were similarly greater in rats fed 2Na-Suc compared to Na-Suc. In addition, there was a tendency toward increased spermidine/spermine N1-acetyltransferase activity in the urinary bladder epithelium of rats fed 5% 2Na-Suc. The results of Experiment 2 corresponded to differences in promoting activity for the different chemicals in Experiment 1. Thus, tumor growth was associated with sodium ion concentration level under conditions of equal increase of urinary pH.

Animals↗
PubMed1982

Sodium transport effects on the basolateral membrane in toad urinary bladder.

In toad urinary bladder epithelium, inhibition of Na transport with amiloride causes a decrease in the apical (Vmc) and basolateral (Vcs) membrane potentials. In addition to increasing apical membrane resistance (Ra), amiloride also causes an increase in basolateral membrane resistance (Rb), with a time course such that Ra/Rb does not change for 1-2 min. At longer times after amiloride (3-4 min), Ra/Rb rises from its control values to its amiloride steady state values through a secondary decrease in Rb. Analysis of an equivalent electrical circuit of the epithelium shows that the depolarization of Vcs is due to a decrease in basolateral electromotive force (Vb). To see of the changes in Vcs and Rb are correlated with a decrease in Na transport, external current (Ie) was used to clamp Vmc to zero, and the effects of amiloride on the portion of Ie that takes the transcellular pathway were determined. In these studies, Vcs also depolarized, which suggests that the decrease in Vb was due to a decrease in the current output of a rheogenic Na pump. Thus, the basolateral membrane does not behave like an ohmic resistor. In contrast, when transport is inhibited during basolateral membrane voltage clamping, the apical membrane voltage changes are those predicted for a simple, passive (i.e., ohmic) element.

Amiloride↗
PubMed1997

Substance P(6-11) and natural tachykinins interact with septide-sensitive tachykinin receptors coupled to a phospholipase C in the rat urinary bladder.

The rat urinary bladder possesses NK1, NK2 (but not NK3) and 'septide-sensitive' tachykinin receptors coupled to a phospholipase C. The present study performed with SR48968 (10(-6) M) to avoid any interaction of the tested peptides with NK2 receptors, indicates that substance P(6-11) (with a high potency), neurokinin A, neurokinin B and to a lesser extent neuropeptide K (with a lower potency) stimulate [3H]-inositol monophosphate ([3H]-IP1) formation in this tissue by acting on the 'septide-sensitive' tachykinin receptors. Substance P(6-11) had little affinity for NK1 binding sites and stimulated [3H]-IP1 formation with an EC50 value and a maximal amplitude similar to those of septide. As previously observed with septide, this maximal response of substance P(6-11) (insensitive to 10(-6) M SR48968) which was about three-fold that of substance P, was blocked by the NK1 receptor antagonist RP67580 and prevented by [Pro9]substance P (NK1 receptor agonist). Similarly, substance P and several substance P C-terminal fragments prevented the substance P(6-11)-evoked response. In addition, neurokinin A, neuropeptide K and neurokinin B induced SR48968-resistant responses which exhibited a maximal amplitude similar to that of substance P (6-11) and were blocked by RP67580 and totally or partially (neuropeptide K) prevented by [Pro9]substance P.

Analgesics↗