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PubMed2004

Regional differences in nitrergic neuronal density in the developing porcine urinary bladder.

Nitric oxide (NO) is involved in normal bladder physiology by regulating local arteriolar tone and smooth muscle relaxation and modulating the production of extracellular matrix proteins in vitro. Little information is available regarding the nitrergic innervation of the bladder during development. In this study we investigated the changes in density and morphology of the intramural nitrergic neurons of the porcine urinary bladder during development using whole-mount preparation. Bladder specimens were obtained from porcine foetuses of gestational age 60 days (n=5) and 90 days (n=5) and from newborn piglets (n=5) after perfusion fixation. Bladders were divided into base, body, and dome. Whole-mount preparation using NADPH-diaphorase (NADPH-d) histochemistry was used to visualize nitrergic innervation of the urinary bladders and to measure density of NADPH-positive ganglia (including single neurons), number of NADPH-d positive neurons per ganglion, and size of individual neurons. One-way ANOVA and chi-square tests were used for statistical analysis with a p-value <0.05 considered statistically significant. NADPH-d positive ganglia were numerous in the muscular layer of all three age groups. At E60, ganglion density was significantly higher in the body (mean 880/cm(2)) than in the dome (397/cm(2)) or the base (676/cm(2)). The ganglion density significantly decreased with age. The number of NADPH-d positive neurons per ganglion increased significantly between E90 and birth (p<0.01). A marked increase in the size of individual neurons over time was also seen (p<0.001), predominantly due to an increase in cytoplasm. Our data on whole-mount preparations demonstrate that significant maturation in nitrergic neuronal density and morphology occurs in the porcine urinary bladder, at least until birth.

Aging↗
PubMedDate not supplied

Beta-adrenergic receptors in the urinary bladder of adult and developing rats.

Specific beta-adrenergic receptors were demonstrated in the urinary bladder of adult and developing rats, by direct tissue binding with LD [125I]-cyanopindolol (CYP). The maximum number of binding sites (Bmax) was 167 +/- 25 fmol/mg membrane protein and the dissociation constant (KD) equalled 61 +/- 33 pM. The Hill slopes of the LD [125I]-CYP binding showed a single class of noncooperative receptor sites. The rank order of potency of agonist competition for LD [125I]-CYP binding suggests that the receptors are mostly of the beta 2 subtype. Beta-adrenergic receptor density was approximately half in the first 10 days of life (Bmax 63 to 77 fmol/mg protein) compared with the older age-groups studied (Bmax 91 to 167 fmol/ng protein). On the 1st day after delivery, the calculated beta-adrenergic receptor number/bladder was 9.4, and it increased significantly with age to 2,496 in the adult rat. This is a 250-fold increase in the number of receptors/bladder, while only a 20-fold increase in membrane protein and a five- to sixfold increase in the bladder weight was observed. Thus, an age-dependent increase of beta-adrenergic receptors on the cell membrane surface area occurred in the developing urinary bladder of the rat.

Adrenergic beta-Antagonists↗
PubMed2004

Immunohistochemical evidence of vanilloid receptor 1 in normal human urinary bladder.

PURPOSE: Experimental and clinical evidences have shown the importance of the vanilloid receptor 1 (TRPV1) in the lower urinary tract. In humans, this receptor has been detected in nerve endings of primary sensory neurons, smooth muscle and connective tissue cells and in the rat also in the urothelium. The aim of this study is to identify, by immunohistochemistry, the cell types expressing TRPV1 in the human urinary bladder. MATERIAL AND METHODS: Specimens, obtained from normal urinary bladder by multiple biopsy and from ureter at the time of radical nefrectomy for renal cell carcinoma, were fixed and frozen. Full-thickness sections were processed for light and fluorescence microscopes. To label the TRPV1, three polyclonal antibodies were used: the anti-capsaicin receptor, the anti-VR1 (N-15) and the anti-VR1 (C-15). RESULTS: Urothelium, smooth muscle cells, mast cells and endothelium were labelled and the labelling was intracytoplasmatic. In the urothelial cells, the labelling was slightly granular. In the bladder urothelium, the superficial cells were more intensely stained than the basal and club-shaped cells. VR1-positive nerve fibers were seen running single and/or in groups in the sub-urothelium and as single varicose fibers in the muscle coat, and VR1-positive nerve endings in the urothelium. CONCLUSION: The present findings provide the evidence of the presence of TRPV1 on normal human urothelium where it could have important implications in the mechanism of action of intravesical vanilloids (capsaicin and resiniferatoxin).

Humans↗
PubMed1990

Suramin antagonizes responses to P2-purinoceptor agonists and purinergic nerve stimulation in the guinea-pig urinary bladder and taenia coli.

1. Suramin, an inhibitor of several types of ATPase, was investigated for its ability to antagonize responses mediated via P2X-purinoceptors in the guinea-pig urinary bladder and P2Y-purinoceptors in the guinea-pig taenia coli. 2. In isolated strips of bladder detrusor muscle, suramin (100 microM-1 mM) caused a non-competitive antagonism of responses to alpha, beta-methylene ATP with an estimated pA2 of approximately 4.7, and inhibited responses to stimulation of the intramural purinergic nerves, with a similar pA2 value. At a concentration of 10 microM, suramin had little effect, but at a concentration of 1 microM, suramin potentiated responses to alpha,beta-methylene ATP, and potentiated responses to electrical stimulation of intramural purinergic nerves. 3. In isolated strips of taenia coli, in which a standard tone had been induced by carbachol (100 nM), suramin at 100 microM and 1 mM significantly antagonized relaxant responses to ATP (at an EC50 concentration) with an estimated pA2 of 5.0 +/- 0.82 and relaxant responses to electrical stimulation of the intramural non-adrenergic, non-cholinergic inhibitory nerves, either single pulses or trains of 8 Hz for 10 s, with estimated pA2 values of 4.9 +/- 0.93 and 4.6 +/- 1.01, respectively. Suramin had no significant effect at 1 or 10 microM. 4. Suramin, at any of the concentrations tested, did not affect contractile responses to histamine (10 microM) or carbachol (10 microM) in the bladder detrusor preparations. In the taenia coli, suramin did not affect either the relaxant responses to noradrenaline (at an EC50 concentration) or the contractile responses to carbachol (100 nM). 5. Thus, suramin at concentrations above 10 microM blocked actions mediated via P2x- and P2y-purinoceptors in the guinea-pig urinary bladder and taenia coli respectively. Potentiation of purinoceptor-mediated activity was seen only at a low concentration of suramin (1 microM) and only in the urinary bladder (P2x-purinoceptor). For its antagonistic activity suramin did not discriminate between P2X- and P2y-purinoceptors, but it was selective for P2-purinoceptor-mediated activity rather than that mediated via cholinoceptors, adrenoceptors or histamine receptors.

Adenosine Triphosphate↗
PubMed2002

Cyclo-oxygenase- and capsaicin-sensitive afferent fibres affect Beta-adrenoceptor-evoked response in the rat urinary bladder.

As reported previously, the beta-adrenoceptor-evoked response in the in vitro rabbit detrusor is inhibited by non-steroidal anti-inflammatory drugs (NSAIDs). Prostaglandins can restore this response. This study was designed to better define physiological influences on beta-adrenoceptors in the urinary bladder and to ascertain whether the observations made in the rabbit urinary bladder in vitro were valid in vivo, as well as in a different animal species, i.e. in the rat. The NSAID indometacin partially inhibited the isoproterenol-evoked response in the rat detrusor muscle. When the neurokinin A (NKA) antagonist MEN-10376 was administered after indometacin, the beta-adrenoceptor-evoked response was completely abolished. The isoproterenol-evoked beta response was dose dependently reduced following treatment with the capsaicin antagonist ruthenium red. Taken together, these data indicate an involvement of prostanoids, NKA- and capsaicin-sensitive fibres in the beta-adrenoceptor-evoked response in the rat urinary bladder.

Adrenergic beta-Agonists↗
PubMed2006

Does the cystometric filling rate affect the afferent bladder response pattern? A study on single fibre pelvic nerve afferents in the rat urinary bladder.

AIMS: To study the effect of physiological and supraphysiological filling rates on the response pattern of single fibre pelvic nerve afferents of the rat urinary bladder. MATERIALS AND METHODS: A total of 37 single afferent bladder units were identified electrophysiologically and their mechanosensitive properties studied. Afferent activity of 13 units was studied at filling rates of 40 and 200 microl/min. Afferent activity of the other units was studied at 200 and 400 microl/min. RESULTS: At the physiological filling rate of 40 microl/min two clearly different types of response pattern were noted. However, at higher supraphysiological filling rates, all units exhibited nearly the same pattern. The difference in mechanosensitive properties of the units that showed a change in response pattern at the supraphysiological filling rate, was characterized by a decrease in pressure at which afferent firing rate peaked. For all units it was found that an increase in filling rate induced an increase in the activation pressure threshold for afferent units, whereas the afferent firing rate at all pressures decreased. CONCLUSIONS: In rats supraphysiological filling rates delay afferent activation, lower afferent firing activity and even change the characteristics of some afferents completely. These data may elucidate some of the differences between ambulatory and conventional urodynamics observed in man.

Animals↗
PubMed1987

Small cell undifferentiated carcinoma of the urinary bladder. A light-microscopic, immunocytochemical, and ultrastructural study of 12 cases.

The clinicopathologic, immunocytochemical, and ultrastructural features of 12 small cell undifferentiated carcinomas (SCUCs) of the urinary bladder are herein reported. The patients ranged in age from 50 to 82 years (median, 76 years). Ten patients were male and two were female. Gross hematuria was the most frequent complaint (67%). Five patients died of disease (median survival, 4 months), three patients are still living with unresectable disease after 6, 10, and 12 months, and four patients were only recently diagnosed. Grossly, most of the tumors were large polypoid masses. On light-microscopic examination, they resembled the intermediate and oat cell variants of pulmonary SCUC. Eight SCUC were associated with other forms of in situ or invasive carcinoma, including transitional cell carcinoma (seven cases), adenocarcinoma (three cases), squamous cell carcinoma (three cases), spindle cell carcinoma (one case), and atypical carcinoid tumor (one case). Immunocytochemically, 11 of the 12 tumors expressed one or more epithelial cell markers (epithelial membrane antigen, human milk fat globule protein-2, cytokeratin). Eleven of the 12 SCUCs were also positive for one or more neuroendocrine markers (neuron specific enolase, chromogranin, Leu-7, vasoactive intestinal polypeptide, serotonin). Electron microscopy performed on seven tumors demonstrated dense-core granules (150-250 nm) in all cases, with tonofilaments in four cases, dendrite-like processes in two cases, and intercellular lumina in one case. The clinicopathologic features of 18 previously reported SCUC of the urinary bladder are also reviewed. SCUC arising in this location is an aggressive neoplasm that often demonstrates multidirectional differentiation, including the frequent but not invariable expression of neuroendocrine features.

Aged↗
PubMed1993

ATP-sensitive potassium channels in smooth muscle cells from guinea pig urinary bladder.

We explored the possibility that ATP-sensitive potassium (KATP) channels exist in urinary bladder smooth muscle, since synthetic openers (e.g., lemakalim) of KATP channels in other tissues relax bladder smooth muscle. Unitary currents through single potassium channels and whole cell potassium currents were measured in smooth muscle cells isolated from the detrusor muscle of the guinea pig bladder. Lemakalim (10 microM) increased whole cell K+ currents by 50 pA at -80 mV with 60 mM external K+ when the cells were dialyzed with 0.1 mM ATP and 140 mM K+. Glibenclamide (10 microM), a sulfonylurea blocker of KATP channels in other tissues, inhibited the entire lemakalim-stimulated current as well as 19 pA of the steady-state K+ current. Glibenclamide-sensitive K+ currents were not dependent on voltage. Increasing intracellular ATP from 0.1 to 3.0 mM reduced the glibenclamide-sensitive K+ current in both the presence and absence of lemakalim by about fourfold. External barium (100 microM) which blocks KATP channels in skeletal muscle reduced KATP channel currents in bladder smooth muscle by 50% at -80 mV. Lemakalim (10 microM) increased the open-state probability of single K+ channels in outside-out patches (with 0.1 mM internal ATP) by sixfold. The single-channel conductance was approximately 7 pS at 0 mV with a physiological K+ gradient. This single-channel conductance was in accord with estimates of conductance made from noise analysis of the lemakalim-induced whole cell current. Glibenclamide inhibited these channels. The number of channels per cell was estimated to be approximately 425. We conclude that urinary bladder smooth muscle has KATP channels and that these channels can be opened by the K+ channel opening drug, lemakalim, and blocked by external glibenclamide and barium. We propose that modulation of these channels may regulate bladder contractility.

2,4-Dinitrophenol↗
PubMed1990

Species differences in sodium o-phenylphenate induction of urinary bladder lesions.

The effects of sodium o-phenylphenate (Na-OPP) treatment on urinary bladder epithelium were examined in male F344 rats, B6C3F1 mice, Syrian golden hamsters and Hartley guinea pigs. Na-OPP was incorporated into diet at a dose of 2% and administered for 4, 8, 12, 24, 36 or 48 weeks. Simple and papillary or nodular (PN) hyperplasias were evident on light microscopy and pleomorphic microvilli demonstrated by scanning electron microscopy were only observed in rats, the lesions becoming more advanced with continued chemical feeding. In mice, hamsters and guinea pigs, proliferative lesions relating to Na-OPP administration were not observed. No significant differences in urinary pH, osmolality or crystal formation were apparent between the various animal species. Since carcinogenicity has been demonstrated for Na-OPP in rats but not in mice, the present findings suggest that Na-OPP might not exert urinary bladder carcinogenic potential in hamsters and guinea pigs.

Animals↗
PubMed1985

[Total cystectomy for urinary bladder cancer: clinicopathological study of 95 cases].

Total cystectomy was performed on 95 patients with primary urinary bladder cancer between 1973 and 1983. Histopathological and prognostic studies were reviewed according to the general rules for clinical and pathological studies on bladder cancer. The cancer histological type were transitional cell carcinoma in 87 cases, squamous cell carcinoma in 5 cases, adenocarcinoma in 2 cases, and undifferentiated carcinoma in 1 case. The overall 5-year actuarial survival rate was 36.0%. As for the growth pattern of the bladder cancer, the 5-year survival rates for the patients with papillary non-invasive type (PNT), papillary invasive type (PIT), and non-papillary invasive type (NIT) were 100%, 25.8% and 34.8% respectively. As for the stage, the 5-year survival rates for the patients with pTa, pT1, pT2, pT3a, pT3b, and pT4 were 81.8%, 64.7%, 40.1%, 30.5%, 22.6% and 6.7% respectively. Of 87 patients with transitional cell carcinoma, the 5-year survival rates for the patients with grade 1, grade 2 and grade 3 were 100%, 43.0% and 32.1% respectively. Intramural lymphatic invasion and vascular invasion and intramural histopathological mode of spread were significant indicators of prognosis.

Adenocarcinoma↗
PubMed1993

Carcinoma arising in urinary bladder diverticula: imaging findings in six patients.

OBJECTIVE: Carcinoma arising within urinary bladder diverticula has a poorer prognosis than do neoplasms that originate within the main bladder lumen as a result of early transmural tumor infiltration. Imaging plays an important role in diagnosing and staging the disease. We describe the radiologic findings in six patients with pathologically proved diverticular carcinomas. MATERIALS AND METHODS: We reviewed the records of six patients who had radiologic examinations and surgically confirmed vesical diverticular carcinomas. The examinations included excretory urography in three patients, cystography in three patients, CT in five patients, and MR imaging in one patient. All patients had hematuria. Five patients had transitional cell carcinoma, and one patient had squamous cell carcinoma. RESULTS: Three of the tumors manifested as an intraluminal filling defect within a bladder diverticulum on excretory urograms or cystograms. In one patient, CT scans showed a concentric soft-tissue tumor in a diverticular neck. Correlative cystograms showed only smooth narrowing in this area. CT and MR imaging showed a tumor within a large diverticulum, which was not visualized on cystograms because of obstruction at the diverticular orifice. CONCLUSION: Imaging plays an important role in identifying bladder diverticula as a potential site of occult neoplasm.

Aged↗
PubMed2003

Role of endothelin ETA and ETB receptors in the guinea-pig urinary bladder contraction.

The distribution and function of endothelin receptors in the guinea-pig urinary bladder were examined. Specific [125I]endothelin-1 binding sites with both the endothelin ET(A) and ET(B) receptor subtypes were distributed in the muscle layer. Endothelin-1 elicited a tonic contraction which was inhibited by cyclo(D-Asp-Pro-D-Val-Leu-D-Trp) (BQ123) but not by N-cis-2,6-dimethylpiperidinocarbonyl-L-gamma-methylleucyl-D-1-methoxycarbonyltryptophanyl-D-norleucine (BQ788) and which was inhibited more strongly by a combination of BQ123 and BQ788. Sarafotoxin S6c elicited a contraction which was abolished by BQ788. The concentration of endothelin-1 in the muscle layer was 707.0+/-67.5 pg/g wet weight. Thus, endothelin-1 may regulate muscle tone via both subtypes of endothelin receptors in an autocrine manner in the guinea-pig urinary bladder.

Animals↗
PubMed2001

Primary signet-ring cell carcinoma of the urinary bladder inducing renal failure.

A case of primary signet-ring cell carcinoma of the urinary bladder that was found to have induced renal failure is the second such case reported in the world. Primary signet-ring cell carcinoma of the urinary bladder is a rare histologic variant of adenocarcinoma. The patient died of distant metastasis 8 months after undergoing total cystectomy. The neoplasm had a high stage at diagnosis, so the prognosis was very poor. To improve the prognosis, earlier diagnosis and establishing a regimen of chemotherapy is necessary.

Carcinoma, Signet Ring Cell↗
PubMed1993

[Diagnostic difficulties in spontaneous rupture of the urinary bladder].

A 63-year-old female patient is described with spontaneous rupture of the urinary bladder who was admitted to hospital with signs of diffuse peritonitis. During surgical operation the site of perforation could not be found, and only inflammatory infiltration of the urinary bladder and surrounding tissues was observed. Cystography carried out after the operation revealed the site of perforation only after six hours from the administration of contrast medium. It was sutured during secondary operation. The postoperative course was uncomplicated.

Female↗
PubMed1987

Oxytocin and cAMP stimulate monovalent cation movements through a Ca2+-sensitive, amiloride-insensitive channel in the apical membrane of toad urinary bladder.

The effects of oxytocin and cAMP on ion transport were investigated in toad urinary bladders incubated with Ca2+-free solutions on the apical side. Under these conditions both oxytocin and cAMP markedly stimulated the movements of Na+, K+, Rb+, Cs+, Li+, and NH4+ through a pathway that is insensitive to amiloride. The amiloride-insensitive currents were inhibited by the addition of Ca2+, Sr2+, or Mg2+ to the apical solution. The movement of the monovalent cations was associated with a spontaneous Lorentzian component in the power spectrum of the fluctuation in short-circuit current. The plateau of the Lorentzian component was enhanced by oxytocin and cAMP and was depressed by divalent cations. Methohexital inhibited the stimulation of monovalent cation movements caused by oxytocin. These findings suggest that oxytocin and cAMP activate at least two kinds of ionic channels in the apical membrane of toad urinary bladder: the well-known amiloride-sensitive channel and an amiloride-insensitive channel that allows the movement of several monovalent cations and is blocked by Ca2+ and other divalent cations.

Amiloride↗
PubMed1987

Cholinergic and non-cholinergic components of the inotropism evoked by electric field stimulation in the isolated rat urinary bladder. Influence of some eicosanoids.

The present study explores whether some arachidonic acid (AA) metabolites formed via cyclo-oxygenase or lipoxygenase pathways influence the inotropism of isolated rat urinary bladders evoked by electric field stimulation (EFS), both in presence of or in absence of atropine. The EFS consisted in square wave pulses of 5 Hz, 5 msec duration and supramaximal voltage, applied every 3 min for a period of 10 sec. Acetylsalicylic acid (ASA) at 10(-4) M, decreased around 30% the magnitude of inotropic responses to EFS and prostaglandin E2 (PGE2, partially at 10(-9) M and fully at 10(-8) M), restored control inotropic levels. PGI2 was also active but only at 10(-7) M; whereas PGF2 alpha, at all concentrations tested (10(-9)-10(-7) M), failed to counteract the diminishing effect of ASA. Moreover, dose-response curves for added acetylcholine (ACh) were not modified by ASA. On the other hand, in presence of atropine (10(-5) M), a diminution of around 40% in the magnitude of control responses to EFS, was detected and when ASA (10(-4) M) was added to atropine-exposed preparations, the atropine resistant component of the EFS-evoked inotropism, was reduced around 30%. Although recovering effects of added PGs were again observed, they were not identical to those observed in absence of atropine. Indeed, PGE2 fully restored the magnitude of contractile responses but it did so only at concentrations 10 times higher than without the cholinergic receptor blocker. On the other hand, PGI2 as well as PGF2 alpha, even at 10(-7) M, were devoid of significant influence. In determining whether lipoxygenase products of AA were also able to modulate the EFS-evoked inotropism, tissue preparations were incubated with nordihydroguaiaretic acid (NDGA), an inhibitor of lipoxygenases, and tested for contractile responses to electric stimulation. NDGA (10(-7) M), failed to alter rat urinary bladder inotropic response to EFS, both in presence of or in absence of atropine. Results suggest that the cholinergic, as well as the non-cholinergic components of the EFS-evoked contractions in isolated rat urinary bladders, are modulated by some cyclo-oxygenase formed AA metabolites, particularly certain PGs, like PGE2.

Animals↗