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PubMed1995

Bradykinin B1 receptors in the rabbit urinary bladder: induction of responses, smooth muscle contraction, and phosphatidylinositol hydrolysis.

1. The aim of this study was to analyse the pharmacological characteristics, and second-messenger coupling-mechanisms, of bradykinin B1 receptors in an intact tissue, the rabbit urinary bladder; and to investigate the influence of inhibition of endogenous peptidases on kinin activities. 2. In preparations of rabbit mucosa-free urinary bladder, at 90 min after mounting of the preparations, bradykinin (1 nM-10 microM) evoked contractile responses. In contrast, the B1 receptor-selective agonist [des-Arg9]-BK (10 mM-10 microM) was only weakly active at this time. Contractile responses to [des-Arg9]-BK increased with time of tissue incubation in the organ bath, reaching a maximum after 3 h, when the pD2 estimates were 6.4 +/- 0.3 for bradykinin, and 6.9 +/- 0.2 for [des-Arg9]-BK. 3. Once stabilized, responses to [des-Arg9]-BK in the bladder were competitively antagonized by the B1 receptor-selective antagonists [Leu8,des-Arg9]-BK and D-Arg-[Hyp3,Thi5,D-Tic7,Oic8,des-Arg9]-BK ([des-Arg10]-Hoe140) (pKB estimates were 6.1 +/- 0.1 and 7.1 +/- 0.1, respectively; n = 17-21), but responses were unaffected by the B2 receptor-selective antagonist D-Arg-[Hyp3,Thi5,D-Tic7,Oic8]-BK (Hoe140) (100 nM; n = 4). Contractile responses to bradykinin itself were partially, but significantly, inhibited by the B1 receptor-selective antagonist, [Leu8,des-Arg9]-BK (10 microM) (P < 0.05), or by the B2 receptor-selective antagonist Hoe140 (100 nM) (P < 0.005) alone, and were largely blocked by a combination of the two antagonists (P < 0.0001). 4. The combined presence of the carboxypeptidase inhibitor DL-2-mercaptomethyl-3-guanidinoethylthiopropanoicacid (mergetpa; 10 microM), the neutral endopeptidase inhibitor, phosphoramidon (1 microM),and the angiotensin-converting enzyme inhibitor, enalaprilat (1 microM) increased the potency of bradykinin17 fold (P<0.001), but that of [des-Argl-BK was unchanged (P>0.05): pD2 estimates were 7.6 +/- 0.1 and 6.8 +/- 0.1 for bradykinin and [des-Argl-BK, respectively, in treated preparations. In the presence of peptidase inhibitors, the affinities of the antagonists [Leu8,des-Arg9]-BK and [des-Arg'j-Hoel4O were unchanged as compared with those determined in the absence of peptidase inhibitors (P> 0.05).[Leu8,des-Argj-BK inhibited responses to bradykinin under these conditions (n = 4).5. In endothelium-denuded preparations of the rabbit isolated aorta, an archetypal B1 receptor preparation,contractile responses to the B1 receptor-selective agonist [des-Argl-BK (10nM- 1O0 AM) (and to bradykinin) increased progressively with time of tissue incubation; and [des-Argl-BK responses were completely antagonized by the B. receptor antagonist [Leu8,des-Arg9]-BK (pKB 6.3 +/- 0.2; n = 13).6. In experiments measuring stimulation of hydrolysis of phosphatidylinositol in rabbit urinary bladder,[des-Argl-BK (10 microM- 1 mM), and bradykinin (100 microM) significantly increased accumulation of inositol phosphates (P<0.0001). The increase in accumulation of inositol phosphates evoked by [des-Arg9]-BK(10 microM - 1 mM) was significantly inhibited by [des-Arg'j-Hoe 140 (10 microM) (P <0.01).7. We conclude that in the mucosa-free rabbit urinary bladder, [des-Argl-BK evokes contraction largely via activation of B1 receptors which have similar properties, including time-dependent induction,to B1 receptors in the rabbit isolated aorta. Bradykinin evokes contraction via stimulation of both B1 and B2 receptors, but does not require conversion by peptidases in order to activate B1 receptors. We demonstrate, for the first time, B1 receptor-coupling to phosphatidylinositol hydrolysis in an intact tissue preparation.

Amino Acid Sequence↗
PubMed1993

Combined trypan blue and glyoxylic acid-induced catecholamine fluorescence in the female rat urinary bladder after distension.

The effect of short-term urinary bladder distension on bladder perfusion and adrenergic innervation was studied in Sprague-Dawley rats. Distension was induced for three hours by forced diuresis and balloon obstruction. A 2% solution of trypan blue was injected into the tail vein 12, 24, 36 and 48 hours after distension and the animals were killed 5-10 min after the injection. Whole thick biopsies were taken from the dome, anterior body and base. A combination of trypan blue and catecholamine fluorescence (GIF method) was used to correlate the distension induced changes in blood vessel perfusion and permeability with changes in adrenergic innervation. Both ischaemic damage and adrenergic hypoinnervation were observed after distension. Later marked extravasation of trypan blue was observed in the whole bladder after 12 hours and after 24 hours distension the dome was almost necrotic in appearance and highly ischaemic. After 36 hours a few exploded small, intensely fluorescent cells (SIF cells) were found to be scattered along the blood vessels, and degranulated mast cells had invaded the anterior body and dome. The adrenergic hypoinnervation reached its maximum 48 hours after distension. The hypoinnervation and possibly also the damage to SIF cells, would seem to be related to ischaemia during distension, probably attributable in turn to overstretching of the organ and its blood vessels. This may provide an explanation for the prolonged micturition problems found after bladder overdistension.

Adrenergic Fibers↗
PubMed2004

Tumor grade-dependent alterations in the protein kinase C isoform pattern in urinary bladder carcinomas.

OBJECTIVES: Members of the protein kinase C (PKC) isoenzyme family play central role in the tumorigenesis of several tissues. In this study our goal was to determine the possible alterations in the protein kinase C (PKC) isoform pattern in relation with the different tumor grade in human urinary bladder carcinomas. METHODS: Western blot analysis, followed by quantitative densitometry, was performed to define the expression of PKC isoforms in the epithelial tissue of human urinary bladder carcinomas with various tumor grades and in control samples. RESULTS: The human urinary bladder epithelium expressed five PKC isoforms (PKC alpha, beta, delta, zeta), the levels of which differentially altered as a function of tumor grade. Namely, whereas the expressions of PKC beta and delta decreased with increasing grade of the carcinomas, the levels of PKC alpha, and zeta showed opposite patterns of changes. CONCLUSIONS: These grade-dependent alterations in the PKC isoform pattern strongly argue for the central yet antagonistic roles of certain members of the PKC system in malignant transformation of human urinary bladder epithelium.

Blotting, Western↗
PubMed1998

Two cases of vasculitis of the urinary bladder: diagnostic and pathogenetic considerations.

BACKGROUND: Vasculitis involving the urinary bladder is rare and difficult to diagnose. Organ-isolated vasculitis challenges pathogenetic theories. METHODS AND RESULTS: A human immunodeficiency virus- and hepatitis B virus-infected man with hematuria and a mass lesion was initially given a clinicopathologic diagnosis of bladder hamartoma. Over 11 months, without immunosuppressive therapy, there were multiple "recurrences" of the tumor with progressive distal ureteral obstruction, but no evidence of systemic vasculitis. Polyarteritis nodosa-like vasculitis with positive immunostaining for hepatitis B surface antigen in urothelium and vessels was found on review. A second patient, presenting with signs and symptoms suggesting transitional cell carcinoma in situ, was found to have small vessel vasculitis. CONCLUSIONS: Bladder vasculitis should be considered in the differential diagnosis of neoplasia. Extrahepatic hepatitis B virus infection may be related to the organ specificity in some cases of vasculitis.

Adult↗
PubMed2003

Effects of urinary bladder distension on activity of T3-T4 spinal neurons receiving cardiac and somatic noxious inputs in rats.

The aims of this study were to examine effects of urinary bladder distension (UBD) on T(3)-T(4) spinal neurons receiving cardiac and somatic noxious inputs and to determine the pathway involved in transmitting urinary bladder inputs to thoracic spinal segments. Extracellular potentials of single T(3)-T(4) neurons were recorded in pentobarbital anesthetized male rats. Either bradykinin solution (10(-5) M) or an allogenic mixture (adenosine 10(-3) M, bradykinin, histamine, serotonin, prostaglandin E2 10(-5) M each) was administered intrapericardially. UBD was produced by saline inflation (0.5-2.0 ml, 20 s). Of 487 neurons tested for responses to UBD, 70 were inhibited and 37 were excited. Seventy-six out of 336 neurons received convergent input from UBD and heart; 69/76 viscerovisceral convergent neurons had somatic fields. Spinal transection at rostral C(1) abolished UBD inhibition in 5/9 neurons; whereas transections at L(1)-L(2) abolished UBD inhibition in 3/3 cells tested. Results showed that T(3)-T(4) spinal neurons processing cardiac and somatic nociceptive information were primarily inhibited by input from the urinary bladder through either supraspinal structures or direct intraspinal pathways.

Action Potentials↗
PubMed1994

Evidence for an inhibitory 5-HT4 receptor in urinary bladder of rhesus and Cynomolgus monkeys.

1. The present study shows that 5-hydroxytryptamine (5-HT) inhibits electrically-evoked contractions of isolated urinary bladder strips from Rhesus and Cynomolgus monkeys via activation of 5-HT4 receptors. 2. 5-HT (0.1 nM-10 microM) produced concentration-dependent inhibition of the contractile response to electrical stimulation yielding a pEC50 of 7.8 (Rhesus monkey) and 7.6 (Cynomolgus monkey). This action of 5-HT was mimicked by 5-methoxytryptamine, renzapride and BIMU 8, each of which behaved as a full agonist relative to 5-HT. However, the potency estimate for BIMU 8 (pEC50 = 6.5) in Cynomolgus monkey was low, relative to 5-HT, indicating a possible heterogeneity of 5-HT4 receptors. 3. The inhibitory action of 5-HT was resistant to antagonism by methysergide (1 microM) and ondansetron (5 microM), thereby eliminating a role for 5-HT1, 5-HT2 and 5-HT3 receptors. The 5-HT4 receptor antagonists, GR 113808 (10 nM), DAU 6285 (1-10 microM) and RS 23597-190 (1 microM), produced parallel, dextral displacements of the concentration-effect curves to 5-HT and other related agonists with affinity estimates in agreement with those defined previously in other 5-HT4 receptor assay systems. 4. Experiments using direct electrical stimulation of bladder smooth muscle indicate that the 5-HT4 receptors are located post-junctionally. 5. The inhibitory action of 5-HT in isolated urinary bladder of monkey differs from the excitatory effect of 5-HT in urinary bladder of man. Species variation and its implications for the development of therapeutic agents are discussed.

Animals↗
PubMed1980

Degeneration analysis of the efferent nerves to the urinary bladder in the cat.

The extrinsic efferent nerve fibres to the urinary bladder in the cat were studied by secondary degeneration after transection of the seventh lumbar, all three sacral and the first coccygeal ventral roots of spinal nerves and after extirpation of both hypogastric ganglia. Under the electron microscope, degenerated nerve fibres of spinal origin could be observed in the trigone region among the ganglion cells and all layers and in the different areas of the urinary bladder wall. These degenerated nerve fibres containing mainly clear vesicles, 30-60 nm in diameter, and a few 80- to 120-nm granular vesicles were situated in synapsing contacts on the surface of the local nerve cells and in synapsing with other probably local nerve processes. After extirpation of the hypogastric ganglia several degenerated nerve fibres could be found along the blood vessels and lymph vessels in all layers. However, occasionally on the surface of the local nerve cells degeneratd nerve fibres could also be found. 2 months after both interferences most of the nerve fibres and synapses remained unaffected. According to these observations the extrinsic efferent nerve fibres and synapse seem to have a modulatory effect on the local ganglia. The large amount of the local intact synapses suggests that the micturition reflex is not a spinal but a local peripheral reflex.

Animals↗
PubMed2005

Short-term effects of arsenic sulfur in deficits of contractile and relaxant responses on urinary bladder: pharmacological and structural changes.

INTRODUCTION: Our goal was to investigate the effects of arsenic sulfur (AsS) on the detrusor smooth muscle reactivity. MATERIAL AND METHODS: AsS (100 ppm microg/g) in drinking water was administered for 2 weeks to two groups of female Wistar rats. The contractile responses of urinary bladders to electrical field stimulation, carbachol, ATP and KCl, and the relaxant responses to ATP, adenosine and isoproterenol were examined. Urinary bladder strips were collected for light microscopic examination. RESULTS: Our results demonstrate that oral inorganic AsS exposure induced enhanced contractile and reduced relaxant responses in rats. We hypothesize that AsS is involved in deficiencies of isolated urinary bladder in rats. CONCLUSION: These functional and morphological changes may be important as an intermediate link in urinary bladder oncogenesis induced by AsS.

Adenosine Triphosphate↗
PubMed1988

Urothelial atypia and survival rate of 500 unselected patients with primary transitional-cell tumour of the urinary bladder.

In a consecutive series of 500 unselected patients with primary urinary bladder tumours the influence of urothelial atypia on the 5 years survival-rate was examined. All tumours were transitional-cell tumours categorized according to the T-classification. Mucosal biopsies from 7 pre-selected sites were taken at the initial cystoscopy in 391 patients (78%) to identify urothelial atypia. The over-all cumulative 5 years survival-rate was 48%. Submucosal and muscle invasion had major influence on survival, whereas tumour grade was less important. Patients with urothelial atypia fared significantly worse than those with normal bladder mucosa (5 years survival 42% versus 62%). This difference in survival-rate became apparent first after two years of observation. Grade II atypia in the bladder mucosa and grade III (carcinoma in situ) had equal significance assessed by the survival-rates.

Adult↗
PubMed2004

Pseudotumor of urinary bladder.

The case of an old male is presented who had postoperative spindle cell nodule of urinary bladder. This benign condition mimics a sarcoma. However, the treatment modalities and the outcome are entirely different. Inflammatory pseudotumor/PSCN and leiomyosarcoma of the bladder overlap in clinical and immunohistochemical findings but are histologically as well as clinically distinct, correlating with different natural histories. Inflammatory Pseudotumor/PSCN are benign, not prone to metastasize, and is outside the spectrum of low-grade inflammatory sarcoma of urinary bladder.

Aged↗
PubMed1988

Schistosomiasis and sarcoma of the urinary bladder.

A young male patient with schistosomiasis and sarcoma of the urinary bladder is presented. Total cystectomy followed by radiotherapy was performed. The gross appearance, microscopic findings of the tumor and an outline of the disease are discussed.

Adult↗
PubMed1985

Further characterization of bacterial adherence to urinary bladder mucosa: comparison with adherence to anion exchange resin.

Bacterial adherence to anion exchange resin has recently been reported to provide a useful, rapid, in vitro screening assay for identifying putative antiadherence agents. The studies presented in this report provide additional evidence that adherence to anion exchange resin is similar to urinary bladder mucosa adherence. Results are as follows. 1) Heparin inhibits the adherence of Escherichia coli, Klebsiella ozaenae, Proteus mirabilis, Streptococcus fecalis and Pseudomonas aeruginosa to both the mucin deficient bladder and anion exchange resin. 2) Drugs which inhibit E. coli adherence to the bladder also inhibit E. coli adherence to the resin and conversely, drugs which do not effect E. coli adherence to the resin do not affect attachment to the bladder. 3) Extracts from mammalian urinary bladder mucosa prevent E. coli adherence to both the bladder and resin. 4) The ability of heparin to displace preattached bacteria from anion exchange resin is inversely proportional to the time the bacteria are in contact with resin. Similar results were obtained for the ability of heparin to displace bacteria from the bladder. These studies indicate that bacterial adherence to anion exchange resin responds to heparin and other chemical agents in a manner similar to the mucin deficient rabbit urinary bladder. Because of the ease and rapid nature of this in vitro assay, it serves as a useful screen for potential bacterial antiadherence agents and could be used to help elucidate mechanisms of bacterial attachment.

Adhesiveness↗
PubMed1978

Effect of phenacetin and caffeine on the urinary bladder of rats treated with N-butyl-N-(4-hydroxybutyl)nitrosamine.

The effect of phenacetin and caffeine on urinary bladder carcinogenesis in rats treated with N-butyl-N-(4-hydroxybutyl)nitrosamine (BBN) was examined. Animals were given a high or low dose of BBN for 4 weeks and then phenacetin or caffeine was administered for 30 or 32 weeks, respectively. All the animals were examined histologically after 36 experimental weeks. The incidence of papillary or nodular hyperplasia, papilloma, and cancer of the urinary bladder was significantly higher in the groups treated with BBN and then with phenacetin than in those treated with BBN alone, especially with a high dose of BBN. Simple hyperplasia and papillary or nodular hyperplasia developed in the urinary bladder of rats treated with phenacetin alone. Papillary proliferative growth of the renal pelvis was seen in one rat treated with a low dose of BBN and phenacetin. Treatment with caffeine after BBN had no enhancing effect and caffeine alone caused no remarkable changes.

Animals↗
PubMed1999

Function, signal transduction mechanisms and plasticity of presynaptic muscarinic receptors in the urinary bladder.

Presynaptic M1 muscarinic receptors on parasympathetic nerve terminals in rat urinary bladder strips are involved in an autofacilitatory mechanism that markedly enhances acetylcholine release during continuous electrical field stimulation. The facilitatory muscarinic mechanism is dependent upon a PKC mediated second messenger pathway and influx of extracellular Ca2+ into the parasympathetic nerve terminals via L and N-type Ca2+ channels. Prejunctional muscarinic facilitation has also been detected in human bladders. The muscarinic facilitatory mechanism is upregulated in hyperactive bladders from chronic spinal cord transected rats; and the facilitation in these preparations is primarily mediated by M3 muscarinic receptors. Presynaptic muscarinic receptors represent a new target for pharmacological treatment of bladder hyperactivity. If presynaptic facilitation is restricted to the bladder and not present in other tissues then drugs acting at this site might be expected to exhibit uroselectivity.

Acetylcholine↗
PubMedDate not supplied

[Carboplatin and radical radiotherapy in the treatment of locally advanced urinary bladder carcinoma].

Our prospective nonrandomized study included 46 patients with invasive urinary bladder carcinoma of the clinical T3a and b stages. The patients were treated by radical radiotherapy (65 Gy, conventional fractioning) and by Carboplatin (150 mg per week during radiotherapy; total 900 mg). Of 35 patients for whom the response was evaluated, the complete regression of tumor was reached in 85.71% and partial in 5.7% of patients. Hematological toxicity of I and II grade was seen in 36/46 of patients. The average follow-up time was 9 months (interval 4-15), overall one year survival rate was 85%, and disease-free survival was 87%. The results have shown that simultaneous application of radical radiotherapy and Carboplatine promises the improvement in the treatment of the invasive urinary bladder carcinoma, but the short follow-up time does not allow the definitive conclusions.

Adult↗
PubMed1998

Increase of low-affinity neurotrophin receptor p75 and growth-associated protein-43 immunoreactivities in the rat urinary bladder during experimentally induced nerve regeneration.

PURPOSE: Nerve regeneration in the urinary bladder after pelvic nerve plexus injury remains uncertain. The objectives were to establish a rat model of nerve regeneration in the bladder and to examine possible changes of low-affinity neurotrophin receptor p75 and growth-associated protein-43 (GAP-43) immunoreactivities during denervation and nerve regeneration. MATERIALS AND METHODS: Adult male rats were divided into 3 groups: controls, crush of the nerve bundles from the right major pelvic ganglion (MPG) to the bladder (nerve crush group) and removal of the right MPG (MPG removal group). Bladders were collected at 3, 7, 14, 30 and 60 days, and immunohistochemically stained for protein gene product 9.5 (PGP9.5: an axonal marker), p75 and GAP-43. RESULTS: In the nerve crush group, PGP9.5 positive nerves were decreased in number at 3 and 7 days, and then increased after 14 days in the muscle layer of the operated side. By 60 days, the density returned to control levels. However, MPG removal resulted in a decrease of the density of PGP9.5 positive nerves throughout the experimental periods. These findings indicate that nerve regeneration occurred in the nerve crush group. The density of p75 labeled fibers was significantly increased at 3 to 30 days postoperatively in the nerve crush group. p75 immunoreactivity showed smooth surface and cytoplasmic staining, indicating that Schwann cells were p75 positive. GAP-43 labeled fibers showed significantly greater density at 3 to 14 days postoperatively. Schwann cells were GAP-43 immunoreactive and, in particular, regenerating nerve fibers appeared to be GAP-43 positive at 14 days. CONCLUSION: The present study suggests that p75 and GAP-43 are involved in the mechanism(s) of nerve regeneration in the urinary bladder.

Animals↗
PubMed1994

M1 muscarinic receptor-mediated facilitation of acetylcholine release in the rat urinary bladder.

1. Release of [3H]ACh in response to electrical field stimulation (10 Hz) was measured in strips of rat urinary bladder and cardiac atrial tissues previously incubated with [3H]choline. 2. The volley output of [3H]ACh release was positively correlated with frequency of stimulation in the urinary bladder but negatively correlated in the atrium. 3. The quantity of [3H]ACh release was influenced by the pattern and duration of stimulation. Continuous stimulation (CS) with trains of 100 shocks released 10 times larger amounts of ACh than the same number of shocks presented as short trains of intermittent stimulation (IS): ten shocks per train with 5 s inter-train intervals. 4. The facilitation of transmitter release was antagonized completely by the administration of atropine (1 microM) or pirenzepine (0.05 microM), a selective M1 antagonist. Eserine, an anticholinesterase agent, markedly facilitated ACh release induced by CS and IS. This effect was blocked by atropine. 5. Release of ACh from atrial strips did not exhibit CS-induced facilitation. Eserine decreased IS- and CS-evoked ACh release in the atrium. 6. It is concluded that continuous stimulation of postganglionic cholinergic nerves in the rat urinary bladder leads to the activation of M1 muscarinic, facilitatory presynaptic receptors which enhance the release of ACh. Presynaptic facilitation may be an important mechanism for modulating neural input to the bladder during micturition.

Acetylcholine↗