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PubMed1988

Comparison of long-term and short-term stretch on rat urinary bladder in vitro.

Distension of the human urinary bladder often causes prolonged impairment of its function. To investigate the effects of the duration of stretch on bladder smooth muscle the active length-tension relation, electrically evoked, was described in rat detrusor strips during a short-term and a long-term stretch. The amplitude of active tension increased at first and then decreased abruptly at greater stretch lengths, the maximum being at muscle lengths 230-250% (100% = resting length) in both types of stretches. When the strips had been at maximum length (300%) for three hours the amplitude was significantly decreased during release as compared to the amplitude found during stretch to the maximum length at comparable lengths. If the strips were released immediately from the maximum length the amplitude responded in an opposite manner. Therefore we conclude that the duration of stretching of bladder smooth muscle significantly affects its mechanical activity.

Animals↗
PubMed1988

Capsaicin-sensitive afferents in the rat urinary bladder activate a spinal sympathetic cardiovascular reflex.

In urethane-anesthetized rats with an intact spinal cord, application of capsaicin on the outer surface of the urinary bladder produced a transient bradycardia, hypotension and negative cardiac inotropism which were neither prevented by i.v. atropine (0.5 mg/kg) nor by cervical vagotomy. In acute spinal rats (C2-C3) application of capsaicin (0.2 and 2 micrograms in 25 microliters) on the urinary bladder induced a transient hypertension, tachycardia and positive cardiac inotropism. A second application (30 min later) induced minor cardiovascular effects, expecially with the higher dose, indicating desensitization. All cardiovascular responses to topical capsaicin were abolished by systemic capsaicin desensitization (50 mg/kg s.c., 4 days before). The excitatory cardiovascular response to capsaicin in acute spinal rats was markedly reduced by bilateral section of pelvic but not hypogastric nerves. Further, it was abolished by pretreatment with hexamethonium (20 mg/kg i.v.) or reserpine (5 mg/kg i.p., 2 days before) and reduced, at various extent for the different components, by phentolamine (0.5 mg/kg i.v.) or propranolol (1 mg/kg). In rats with pelvic and hypogastric nerves intact, section of the cord at a level (T12-L1), just above the medullary segments which receive primary afferent input from the bladder (L6-S1), abolished the excitatory cardiovascular response to application of capsaicin on the bladder. In spinal rats (C2-C3) rapid distension of the urinary bladder with saline produced transient tachycardia, hypertension and positive cardiac inotropism similar to that evoked by capsaicin.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMedDate not supplied

Genetically determined sparteine oxidation and sulfadimidine acetylation polymorphism in patients with non-occupational urinary bladder cancer.

The results of our study revealed a predominance of the percentage of extensive metabolizers (EM) of sparteine (94.8%) among 58 patients with non-occupational urinary bladder cancer in comparison with the percentage of extensive metabolizers (91.2%) in healthy persons; the difference being not statistically significant. However, among ultrarapid (EM) oxidators with the metabolic ratio (MR) < 0.5 the difference in the MR frequency distribution between 15 patients with bladder cancer (25.9%) and 18 healthy persons (11.25%) was statistically significant. Therefore, our studies provide some evidence of a possible relationship between the EM sparteine oxidation phenotype and the susceptibility to non-occupational bladder cancer. Not statistically significant slight prevalence of the percentage of slow acetylators (SA) (53.1%) among 32 urinary bladder cancer patients in comparison with the percentage of SA (49%) among 45 healthy persons may confirm the conclusion that a slow acetylator phenotype is not associated with the increased risk of the development of non-occupational urinary bladder cancer.

Acetylation↗
PubMed1999

Mitochondrial and mitochondrial-related nuclear genetic function in rabbit urinary bladder following reversal of outlet obstruction.

Partial outlet obstruction of the rabbit urinary bladder causes increased tissue hypertrophy and decreased contractility of that organ; we showed that, in an experimental rabbit model, both correlate closely with alterations in the status and expression of mitochondrial (mt), and mt-related nuclear, genetic parameters in bladder smooth muscle. Here we investigate the rate and overall level of recovery of mt and nuclear genetic function following reversal of outlet obstruction in the same animal model. Release from outlet obstruction at 28 days resulted in improvement in both level of hypertrophy and contractile function in all bladders studied. However, bladders fell into two groups based on whether relative copy mt genome number per cell was above or below that of unobstructed controls. Bladders with high mt DNA content adjusted organellar genome copy number toward normal post-reversal but did not properly adjust mt transcript levels; mt-related nuclear transcripts in these samples showed recovery. Bladders with low mt DNA content showed no adjustment of those levels toward normal post-reversal but did show some adjustment in other mt and nuclear genetic parameters. Thus, a limiting factor for return of normal bladder function following reversal of outlet obstruction may be recovery of normal mt genetic performance.

Animals↗
PubMed1990

Spindle cell lesions of the urinary bladder.

Spindle cell proliferations of diverse types which vary greatly in their behavior may occur in the urinary bladder. Some of them such as the inflammatory pseudotumor and the postoperative spindle cell nodule are reactive and clinically benign although they may be responsible for significant symptoms. On the other hand, certain other lesions such as sarcomatoid carcinomas are typically highly malignant tumours. The features of the inflammatory pseudotumor and postoperative spindle cell nodule have only recently been defined. The tendency of the former to occur in young patients and the association of the latter with a recent operative procedure are important pieces of clinical information which may prevent their mis-diagnosis. The diagnosis of sarcomatoid carcinoma should always be considered when a malignant spindle cell proliferation is encountered in the urinary bladder. Careful search for minor foci of obvious epithelial differentiation is important in establishing the diagnosis which may also be aided by immunohistochemical staining for epithelial markers. Sarcomatoid carcinoma should be distinguished from the rare transitional cell carcinoma with pseudosarcomatous stroma and from carcinosarcoma. The final lesions briefly reviewed here are mesenchymal tumors both benign and malignant, which generally do not pose the same degree of diagnostic difficulty as non-neoplastic mesenchymal proliferations and sarcomatoid carcinomas.

Carcinoma↗
PubMed1978

The WHO histological classification of urinary bladder tumours.

The WHO histological classification of urinary bladder tumours was formulated to promote better international communication and more reliable statistical comparisons. The axes of classification concern histological type, grade of anaplasia and growth pattern.

Humans↗
PubMed1997

[Genomic changes in urinary bladder cancer].

Recent molecular studies on transitional cell carcinomas (TCC) of the urinary bladder suggest two genetically different tumor types with a varying degree of genomic instability-pTa (grade 1 and 2) tumors are usually "genetically stable". These tumors have rarely p53 alterations and contain only few genomic alterations (deletions, DNA sequence copy number gains, amplifications). Genomic changes in these tumors typically include losses of the chromosomes Y and 9 as well as 1q gains. TCC's with invasive growth pattern (pT1-4) are mostly "genetically instable". They have p53 alterations in about 50% of tumors, and often numerous DNA sequence copy number changes including deletions of 2q, 5q, 6q, 8p and 11p as well as gains at 1q, 3p, 3q, 5p, 6p, 8q und 10p. High level amplifications at various sites of the genome are also frequent in these "instable tumors". They may pinpoint the localization of overexpressed oncogenes. Further studies will have to investigate whether genetic analyses can add useful information to the currently used pathological (pTNM) and clinical (superficial/invasive) classifications of urinary bladder cancer.

Carcinoma, Transitional Cell↗
PubMed2005

Differences in susceptibility to N-butyl-N-(4-hydroxybutyl)nitrosamine-induced urinary bladder carcinogenesis between SD/gShi rats with spontaneous hypospermatogenesis and SD/cShi rats with spontaneous hydronephrosis.

Differences in susceptibility to N-butyl-N-(4-hydroxybutyl)nitrosamine (BBN)-induced urinary bladder carcinogenesis between two substrains of male Sprague-Dawley rats were examined. One substrain was SD/gShi, which has spontaneous hypospermatogenesis, and the other was SD/cShi, which is a sister strain of SD/gShi, and has normal testis but spontaneous hydronephrosis. SD/gShi rats had a lower incidence of urinary bladder tumors and had lower 5-bromo-2'-deoxyuridine labeling indices in the urinary bladder epithelium than SD/cShi rats when BBN was given. SD/gShi rats had significantly lower urinary concentrations of N-butyl-N-(3-carboxypropyl)nitrosamine (BCPN), which is a metabolite and proximate carcinogen of BBN. In vitro analysis also showed significantly less BCPN formation, using an S9 mix derived from the liver and kidney, in SD/gShi rats than in SD/cShi rats. BCPN formation in vitro was markedly inhibited by non-selective cytochrome P450 (CYP) inhibitors, but not alcohol dehydrogenase inhibitor. However, analysis of CYP proteins including hepatic CYP1A1/2, 2B1/2, 2E1, and 3A2 and renal CYP2E1 and 3A2 revealed no significant variation in levels in either tissue in the groups. There were also no significant intergroup differences in the mutagenicity of carcinogens, including heterocyclic amines and N-nitrosamines, activated by CYP1A1/2 and CYP2E1 and/or CYP2B1/2, respectively. These results suggest that SD/gShi rats are less susceptible to BBN, possibly because less BCPN is produced by CYP isoforms other than those investigated. A contribution of CYP4B1 to the strain difference is also possible.

Animals↗
PubMed2001

Staging and terminology of superficial urinary bladder tumors.

Ta and T1 transitional cell urinary bladder tumors are prone to recurrence in a large percentage of cases, but they uncommonly progress to invasive tumors. On the other hand, Tis bladder tumors progress to invasive tumors in a majority of cases. Even though all of these tumors are found in the superficial layers of the bladder wall, their natural histories are significantly different. In addition, new terminology has been developed for these lesions.

Carcinoma, Transitional Cell↗
PubMed1993

Differential changes of adrenoceptor- and muscarinic receptor-linked prostacyclin synthesis by the aorta and urinary bladder of the diabetic rat.

1. The effect of experimental diabetes mellitus (DM; hyperglycaemic, non-ketototic; 2 months duration) in the rat on receptor-linked prostacyclin (PGI2) synthesis (measured as 6-oxo-PGF1 alpha by radioimmunoassay) was studied in the aorta and urinary bladder using adrenaline, angiotensin II (AII) and acetylcholine (ACh). Signal transduction systems were studied via stimulation of PGI2 synthesis with phorbol ester dibutyrate (PDBU; a protein kinase C activator [PKC]), Ca2+ ionophore A23187 (A23187) and thapsigargin (both elevate intracellular Ca2+, activating phospholipase A2 [PLA2]) and arachidonate (AA; substrate for PGI2 synthesis). 2. In response to adrenaline, AII and phorbol ester, aortic PGI2 release was markedly reduced (all > 75%) in diabetic rats compared to controls. EC50s of the dose-response curves for adrenaline, AII and PDBU were also markedly increased in aortae from DM rats compared to controls. Although there was decreased output of PGI2 in response to A23187 by aortae from diabetic rats compared to controls, there was no difference in the EC50s (mean +/- s.e. mean: diabetic, 2.7 +/- 0.2 x 10(-6) M; controls 2 +/- 0.18 x 10(-6) M). There were no differences in PGI2 release (or in the EC50s) in response to thapsigargin or AA between aortae from diabetic and control rats. 3. In the urinary bladder, there was a marked increase in PGI2 output in response to ACh and a marked decrease in EC50s for the ACh-PGI2 dose-response curves in diabetic rats (EC50 = 5.8 +/- 0.32 x 10(-7) M) compared to controls (EC50 = 2.2 +/- 0.15 x 10(-6) M). Although there was an increase in PGI2 output in the urinary bladders from diabetic rats in response to A23187, there were no differences in the EC50s (control, 1.8 +/- 0.2 x 10-6 M; diabetic, 1.1 +/- 0.15 X 10-6 M). In the urinary bladders, there were no differences in PGI2 output (or the EC50s) in response to PDBU, thapsigargin or AA between diabetic or control rats.4. These data indicate that: (i) reduced PGI2 synthesis coupled to adrenoceptors and AII receptors in the aortae of diabetic rats may be due to diminished PKC activity and not to changes in receptor density and/or affinity, Ca2+ stores, PLA2, cyclo-oxygenase or PGI2 synthase; (ii) the diametrically opposite effect of DM on ACh-stimulated PGI2 synthesis is not due to an increase in PKC activity, but possibly to an increase in muscarine receptor number and/or affinity; (iii) changes in receptor-linked PGI2 synthesis are not ubiquitous in experimental DM and may be organ-specific.

Angiotensin II↗
PubMed1988

Regional noradrenergic and cholinergic neurochemistry in the rat urinary bladder: effects of age.

Neurochemistry of the base and body of the rat urinary bladder was compared for both adrenergic and cholinergic parameters using Fischer 344 rats. In bladder base and body, respectively, the concentration (pmol./mg. wet weight) of norepinephrine was 23.4 and 2.16, of acetylcholine was 26.7 and 18.3, and of choline was 96.7 and 199. The activity (nmol./mg. protein/hour) of tyrosine hydroxylase was 422 and less than 50, of monoamine oxidase was 80.6 and 126, of choline acetyltransferase was 17.4 and 11.5, and of acetylcholinesterase (nmol./mg. wet weight/hour) was 485 and 165. Treatment with alpha-methyl-p-tyrosine did not alter norepinephrine concentration in bladder base but decreased it by 27% in bladder body. Studies were also done to determine whether age-related changes exist in the adrenergic and cholinergic neurochemistry of the rat urinary bladder. Bladders from rats of 6-7, 15-17, and 22-24 mo. of age were examined. The only age-related differences noted were a progressive decrease in level of monoamine oxidase activity in both bladder regions and an increase in bladder base norepinephrine concentration from 6-7 to 15-17 mo. followed by a decrease at 22-24 mo. Overall, the results show marked regional variations in bladder neurochemistry which remain remarkably stable as the animals grow old.

Acetylcholine↗
PubMed2007

CD34+ fibrocytes in chronic cystitis and noninvasive and invasive urothelial carcinomas of the urinary bladder.

CD34+ fibrocytes are constitutive elements of the connective tissue where they play a role in matrix synthesis and tumor-associated stromal remodeling. Secreted protein, acidic, and rich in cysteine (SPARC) is a pivotal mediator of stromal remodeling precipitated by invasive carcinomas. The present study was undertaken to investigate CD34+ fibrocytes in the stroma of the tumor-free urinary bladder, chronic cystitis, and urothelial carcinomas together with stromal expression of alpha-smooth muscle actin (alpha-SMA), CD117, and SPARC. In tumor-free urinary bladder and chronic cystitis, CD34+ fibrocytes were found in the deep lamina propria and tunica muscularis, whereas the superficial lamina propria disclosed a CD34-negative and alpha-SMA-positive fibrocyte-like cell. Invasive urothelial carcinomas revealed a complete loss of CD34+ fibrocytes and concomitant appearance of alpha-SMA-reactive myofibroblasts which showed strong expression of SPARC. CD117 expression of tumor-free and tumor-associated stroma revealed no differences. We in this study for the first time describe CD34+ fibrocytes in the urinary bladder and an up-to-now unknown population of alpha-SMA-positive fibrocytes exclusively occurring in the superficial lamina propria. Stromal remodeling associated with invasive carcinomas in the urinary bladder is characterized by a loss of CD34+ fibrocytes paralleled by a gain of alpha-SMA-positive myofibroblasts and increased expression of SPARC.

ADAM Proteins↗
PubMed1999

Late functional response of mouse urinary bladder to fractionated X-irradiation.

PURPOSE: Late functional changes in mouse urinary bladder were studied after fractionated irradiation in order to define parameters of repair of sublethal radiation damage. MATERIALS AND METHODS: In the repair capacity study, 1 to 10 fractions were applied within 5 days. To assess the kinetics of repair, 4 fractions were applied with intervals of 0, 0.5, 1, 2, 4, or 8h. The endpoint used to establish dose-effect relationships was a reduction in the cystometrically measured bladder capacity by > or = 50% of the individual pre-treatment value. Data analysis was performed with a linear-quadratic mixture model, which includes latent-time analysis in an effect-dependent manner. RESULTS: The alpha/beta values were found to be 4.4 Gy (95% confidence interval [2.0-8.4]) for the repair capacity data alone and 3.7 Gy (1.7-6.7) in combination with the repair kinetics data. The half-time of repair, assuming mono-exponential repair kinetics, was 0.39 h (95% CI [0.23-1.3]). The mean latent time decreased from around 40 weeks to 12 weeks, inversely dependent on the biologically effective dose. In animals experiencing an acute response during the first month after treatment, the incidence of severe late responses was significantly increased (p=0.0025). CONCLUSIONS: The present results confirm that the sparing effect in the mouse urinary bladder by dose fractionation is in the lower range of chronically responding tissues. The half-time of repair is in the lower range reported for mouse tissues.

Animals↗
PubMedDate not supplied

Multi-stage carcinogenesis in the urinary bladder.

Sodium saccharin has been shown to be a promoting substance for urinary bladder carcinogenesis in the rat following initiation with N-methyl-N-nitrosourea, N-[4-(5-nitro-2-furyl)-2-thiazolyl]formamide (FANFT), or N-butyl-N-(4-hydroxybutyl)nitrosamine. It has been shown to have many of the properties of promoting substances in other animal models, such as the mouse skin; it lacks mutagenic activity, induces hyperplasia in the target tissue, and does not bind DNA. It has recently been demonstrated to be co-carcinogenic for the rat bladder. It has also been shown that the administration of sodium saccharin during the regenerative hyperplasia observed after freeze ulceration or cyclophosphamide administration resulted in the induction of bladder tumours, even without pre-initiation with FANFT or other known initiating substances. This model appears to be analogous to the administration of sodium saccharin to animals with a rapidly proliferating bladder mucosa as occurs in utero during the two-generation carcinogenesis experiments and in the pellet-insertion experiments in which a cholesterol pellet containing sodium saccharin is inserted into the bladder. To enhance our understanding of the complex interaction of the many variables involved in two-stage bladder carcinogenesis, a stochastic model has been formulated based on long-term carcinogenicity and in vivo tissue kinetic studies. This model indicates the importance of cell proliferation and the development of hyperplasia in carcinogenesis.

Animals↗
PubMed1996

Tachykinin NK-2 receptors in child urinary bladder.

PURPOSE: Although NK-2 receptors mediate contractions to tachykinins in adult detrusor muscle, little is known about the functions of tachykinins in child urinary bladder. Here we have used highly selective agonists and antagonists to examine NK-2 receptors in child detrusor muscle. MATERIALS AND METHODS: Specimens of urinary bladder from 23 children (0 to 10 years0 were obtained at operation for vesicoureteric reflux. Strips of detrusor muscle were mounted in organ baths in Krebs solution containing phosphoramidon (10 microM.), and isometric tension was recorded. Contractile responses were elicited by tachykinins and selective agonists in the presence and absence of autonomic inhibitors and of tachykinin NK-2 receptor antagonists. RESULTS: The NK-2 receptor agonists neurokinin A (NKA), neuropeptide gamma and [Lys5, MeLeu9, Nle10]-NKA(4-10) contracted the isolated child detrusor, with pD2 values of 7.7, 7.2 and 7.3. The maximum response to NKA was greater than that to the other 2 agonists. No age-related differences were seen. Selective agonists for NK-1 receptors ([Sar9, Met(O2)11]-SP and septide) and NK-3 receptors (senktide) were ineffective contractile agents. Responses to NKA were unaffected by phentolamine (5 microM.), propranolol (3 microM.), tetrodotoxin (1 microM.) and indomethacin (1 microM.), indicating a direct action on smooth muscle. The tachykinin NK-2 receptor antagonists SR 48968 and MEN 10627 caused a concentration-dependent antagonism of responses to NKA, with apparent pKB values of 9.4 and 8.1. CONCLUSIONS: Neurokinin A appears to act directly on NK-2 receptors on detrusor muscle of infant and child urinary bladder, without involvement of neural or indirect contractile mechanisms. Potency of antagonists was similar to that seen in other tissues. However, agonist potency was significantly lower in the isolated detrusor from children, compared with our previous study in adult detrusor. This discrepancy may be related to age-related differences in NK-2 receptors or in contractile mechanisms; alternatively it may be a result of the reflux condition.

Child↗
PubMed1994

Urinary bladder hyperplasia in the rat: non-specific pathogenetic considerations using a beta-lactam antibiotic.

Eight of the known chemical substances associated with neoplasia in man are known to target the urinary bladder urothelium. Preneoplastic changes have been identified following exposure to each of these chemicals, and they have also been seen to occur in many species of lab animals. The most important such change is preneoplastic hyperplasia. Adaptive hyperplasia is the first form of hyperplasia to appear. It can be seen both in untreated controls and dosed animals. The distinguishing features are that in treated groups it does not progress with dose or time, and the process is reversible. Reparative hyperplasia involves disruption of homeostasis. Its severity increases with dose and time. It is not seen in controls but it is still reversible during the recovery segment after exposure to a toxic substance. When reparative hyperplasia continues beyond a certain threshold of time and dose, it progresses to preneoplastic hyperplasia, which further progresses with continued stimulation to frank neoplasia. The synthetic beta-lactam penem antibiotic FCE 22891 and its metabolite FCE 22101 caused adaptive urothelial hyperplasia of the urinary bladder only in rats and in no other species. Based on the pharmacokinetic profile of FCE 22891 and FCE 22101, it can be deduced that the morphologic finding of adaptive urothelial hyperplasia is caused by reduction of intravesicular urine pH. This effect has no relevance to therapeutic use in humans. Further, it is important to distinguish adaptive and reparative hyperplasia in preclinical toxicity studies.

Animals↗
PubMed1988

Regulation of [3H]GABA release from strips of guinea pig urinary bladder.

The presence of receptors that regulate the release of gamma-aminobutyric acid (GABA) was studied in strips of the guinea pig urinary bladder. GABA (10(-8)-10(-5) M) and muscimol (10(-8)-10(-5) M), but not baclofen (10(-5) M), reduced the Ca2+-dependent, tetrodotoxin-resistant release of [3H]GABA evoked by high K+ from the urinary bladder strips preloaded with [3H]GABA. The inhibitory effect of muscimol was antagonized by bicuculline and potentiated by diazepam, clonazepam, and pentobarbital sodium. The potentiating effect of clonazepam was antagonized by Ro 15-1788. Acetylcholine (ACh) inhibited the high K+-evoked release of [3H]GABA. The inhibitory effect of ACh was antagonized by atropine sulfate and pirenzepine but not by hexamethonium. Norepinephrine (NE) inhibited the evoked release of [3H]GABA. The inhibitory effect of NE was mimicked by clonidine, but not by phenylephrine, and was antagonized by yohimbine but not by prazosin. These results provide evidence that the release of GABA from strips of guinea pig urinary bladder is regulated via the bicuculline-sensitive GABAA receptor, M1-muscarinic, and alpha 2-adrenergic receptors.

Acetylcholine↗
PubMed1985

On the inotropic effects of leukotrienes in the isolated urinary bladder of guinea pigs and rats.

Leukotrienes (LTs) B4, C4 and D4 were tested on the motility of rings isolated from the urinary bladder of guinea pigs and rats. LTB4 did not evoke inotropic influences in any of the preparations, whereas LTC4 and LTD4 augmented the magnitudes of tonic and phasic contractions in the guinea pig but not in the rat detrusor muscle, LTC4 evoking a greater enhancement than LTD4. On molar bases, acetylcholine induced smaller positive inotropic effects. In the presence of 10(-4) acetylsalicylic acid (ASA), cumulative dose-response curves of phasic and tonic contractions for LTC4 were shifted to the right of controls, whereas curves of the phasic motility for LTD4 remained unaltered. However, ASA shifted to the left the dose-response curve of tonic contractions for LTD4 and in addition evoked an augmentation of the absolute developed tension. The initial (postequilibrium) contractile levels of basal phasic contractions did not differ between controls and preparations incubated with ASA (10(-4) M), nordihydroguaiaretic acid (10(-7) M) or FPL-55712 (3 X 10(-6) M). The findings suggest that some musculo-active prostanoid(s) could be modulating, in opposite directions, the smooth muscle contractile reactivity of the guinea pig urinary bladder when challenged in vitro with LTC4 and LTD4. Our data reported hereing also suggest that the role, if any, of endogenous prostanoids and leukotrienes for the normal basal contractile functioning of the guinea pig urinary bladder, remains obscure.

Animals↗