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At least 127 records · Page 7Linked to original sources
PubMed2000

P2X receptor expression in mouse urinary bladder and the requirement of P2X(1) receptors for functional P2X receptor responses in the mouse urinary bladder smooth muscle.

1. We have used subtype selective P2X receptor antibodies to determine the expression of P2X(1 - 7) receptor subunits in the mouse urinary bladder. In addition we have compared P2X receptor mediated responses in normal and P2X(1) receptor deficient mice to determine the contribution of the P2X(1) receptor to the mouse bladder smooth muscle P2X receptor phenotype. 2. P2X(1) receptor immunoreactivity was restricted to smooth muscle of the bladder and arteries and was predominantly associated with the extracellular membrane. Diffuse P2X(2) and P2X(4) receptor immunoreactivity not associated with the extracellular membrane was detected in the smooth muscle and epithelial layers. Immunoreactivity for the P2X(7) receptor was associated with the innermost epithelial layers and some diffuse staining was seen in the smooth muscle layer. P2X(3), P2X(5) and P2X(6) receptor immunoreactivity was not detected. 3. P2X receptor mediated inward currents and contractions were abolished in bladder smooth muscle from P2X(1) receptor deficient mice. In normal bladder nerve stimulation evoked contractions with P2X and muscarinic acetylcholine (mACh) receptor mediated components. In bladder from the P2X(1) receptor deficient mouse the contraction was mediated solely by mACh receptors. Contractions to carbachol were unaffected in P2X(1) receptor deficient mice demonstrating that there had been no compensatory effect on mACh receptors. 4. These results indicate that homomeric P2X(1) receptors underlie the bladder smooth muscle P2X receptor phenotype and suggest that mouse bladder from P2X(1) receptor deficient and normal animals may be models of human bladder function in normal and diseased states.

Adenosine Triphosphate↗
PubMed2004

Properties of a tonically active, sodium-permeable current in mouse urinary bladder smooth muscle.

Urinary bladder smooth muscle (UBSM) elicits depolarizing action potentials, which underlie contractile events of the urinary bladder. The resting membrane potential of UBSM is approximately -40 mV and is critical for action potential generation, with hyperpolarization reducing action potential frequency. We hypothesized that a tonic, depolarizing conductance was present in UBSM, functioning to maintain the membrane potential significantly positive to the equilibrium potential for K(+) (E(K); -85 mV) and thereby facilitate action potentials. Under conditions eliminating the contribution of K(+) and voltage-dependent Ca(2+) channels, and with a clear separation of cation- and Cl(-)-selective conductances, we identified a novel background conductance (I(cat)) in mouse UBSM cells. I(cat) was mediated predominantly by the influx of Na(+), although a small inward Ca(2+) current was detectable with Ca(2+) as the sole cation in the bathing solution. Extracellular Ca(2+), Mg(2+), and Gd(3+) blocked I(cat) in a voltage-dependent manner, with K(i) values at -40 mV of 115, 133, and 1.3 microM, respectively. Although UBSM I(cat) is extensively blocked by physiological extracellular Ca(2+) and Mg(2+), a tonic, depolarizing I(cat) was detected at -40 mV. In addition, inhibition of I(cat) demonstrated a hyperpolarization of the UBSM membrane potential and decreased the amplitude of phasic contractions of isolated UBSM strips. We suggest that I(cat) contributes tonically to the depolarization of the UBSM resting membrane potential, facilitating action potential generation and thereby a maintenance of urinary bladder tone.

Action Potentials↗
PubMed1989

Identification of epidermal growth factor as a component of the rat urinary bladder tumor-enhancing urinary fractions.

Using the heterotopically transplanted rat urinary bladder, we have shown that normal rat urine has a potent tumor-enhancing effect on bladder carcinogenesis. In an attempt to isolate tumor-enhancing factor(s), urine was fractionated by Bio-Gel P-100 column chromatography and each eluate fraction was examined for inducibility of ornithine decarboxylase (ODC) in a target rat bladder carcinoma cell line, 804G. We have identified two ODC-inducible peaks, one located in a high molecular weight region designated as Fraction I (Fr. I) and the second in a low molecular weight region designated as Fraction II (Fr. II). Fr. I consisted of two principal elements, transferrin and a component which induced ODC. The present investigation was conducted to characterize the ODC-inducible activity in Fr. I and II. Chromatographic analysis of Fr. I by Sephacryl S-200 and Fr. II by Bio-Gel P-10 chromatography separated several ODC-inducible peaks. However, the major ODC inducibility was due to a high concentration (460 ng/mg Fr. I residue, approximate Mr 54,000, and 580 ng/mg Fr. II residue, approximate Mr 6,100) of epidermal growth factor (EGF) as determined by radioimmunoassay. Aliquots obtained from these peaks competed with mouse EGF for EGF receptors in A431 cells. Preincubation of Fr. I and II with rabbit anti-rat EGF IgG significantly reduced ODC inducibility. Transforming growth factor alpha activity as determined by radioimmunoassay was also demonstrated in both Fr. I (34 ng/mg) and Fr. II (9 ng/mg). The results of the present study together with our previous data indicate that the majority of the ODC-inducing activity in the tumor-enhancing urinary components Fr. I and Fr. II is due to EGF itself and EGF-related growth factors of high molecular weight and that Fr. I also contains transferrin.

Animals↗
PubMed1994

Non-adrenergic, non-cholinergic control of the urinary bladder.

In the urinary, bladder, ATP is an excitatory neuromuscular transmitter, possibly a cotransmitter with acetylcholine from postganglionic parasympathetic nerves, which activates P2X-purinoceptors. The synthesis of prostaglandins is closely linked to the activation of P2X-purinoceptors, and these compounds make a significant contribution to non-cholinergic neurogenic responses. Many neuropeptides, such as NPY, VIP, somatostatin, SP and CGRP, are found in nerves innervating the lower urinary tract, but it is unlikely that any is a neuromuscular transmitter in the detrusor; rather, they may act as potent modulators of sympathetic and parasympathetic transmission. Modulatory actions are shown by GABA par excellence; this compound is also well represented in vesicular neurons and, via activation of GABAA- or GABAB-receptors, can potentiate or inhibit parasympathetic transmission. Although not discussed in depth in this review, the urinary bladder shows extraordinary plasticity in expression of nerves and of their transmitters and receptors under pathophysiological conditions, including pregnancy and ageing as well as disease states. Finally, the accessibility of the urinary bladder and the enormous range of chemoreceptors that it possesses has led to its being used extensively for pharmacological investigations of transmitter and drug receptors and their subclasses.

Adenosine Triphosphate↗
PubMed1991

Significance of nonvisualization of the fetal urinary bladder.

The fetal urinary bladder was visualized sonographically in 1254 (94%) of 1335 consecutive fetuses of 14 weeks of development or older, but it could not be seen in 81 cases (6%). Five of these cases were lost to follow-up and were excluded from the study. Of the remaining 76 cases, 69 (91%) of the pregnancies progressed to term, and the infants were normal at birth and at 6 week perinatal follow-up. Seven (9%) of the fetuses had a variety of associated obstetrical abnormalities that resulted in fetal demise or termination of the pregnancy (oligohydramnios, hydrops, intrauterine growth retardation [IUGR], ventriculomegaly, diaphragmatic hernia, cystic hygroma, and triploidy). Notably, none of these were renal tract anomalies. We concluded that (1) nonvisualization of the fetal urinary bladder with an otherwise normal sonogram, including normal volume of amniotic fluid and normal renal areas, is of no clinical concern and does not require follow-up, and (2) nonvisualization of the fetal urinary bladder in the setting of associated obstetrical abnormalities may be secondary to renal tract anomalies or may only be a consequence of the associated abnormalities.

Female↗
PubMed1979

Reversible inhibition by lanthanum of the hydrosmotic response to serosal hypertonicity in toad urinary bladder.

In the urinary bladder of amphibia, hypertonicity of the serosal bath (SH) evokes an increase in transepithelial water permeability, the characteristics of which resemble the response to antidiuretic hormone (ADH). The ionic dependency, in particular for Ca2+, appears very similar for SH- and ADH-induced water fluxes. In the present experiments La3+ was used as a probe to study the Ca2+-dependency of the hydrosmotic response to SH in isolated urinary bladder of the toad Bufo marinus. Addition of La3+ (5 mM) on the serosal side of the membrane produced a significant and reversible increase in basal transepithelial water flux. The hydrosmotic response elicited by adding 250 mM mannitol to the serosal Ringer's solution was inhibited by 30% in the absence of serosal Ca2+. Similarly, the hydrosmotic response to SH was inhibited by 37%, 30% and 40% when 5 mM La3+ was added to the serosal medium 30 min before, concommitantly with, or 60 min after induction of SH. The inhibition of transepithelial water flux observed in the absence of serosal Ca2+ or in the presence of serosal La3+ was reversible. The results support a critical role for Ca2+ in the modulation of transepithelial water permeability in the urinary bladder of amphibia. Ca2+ presumably exerts its effects at a post-cyclic AMP step.

Animals↗
PubMed1989

Correlation between the DNA damage in urinary bladder epithelium and the urinary 2-phenyl-1,4-benzoquinone levels from F344 rats fed sodium o-phenylphenate in the diet.

The relationship between urinary metabolites and DNA damage in the urinary bladder epithelium of male and female rats was tested by alkaline elution assay after an intravesical injection of OPP or its urinary metabolites. 2-Phenyl-1,4-benzoquinone (PBQ) revealed a weak DNA-damaging activity in both sexes at 0.05-0.1%. OPP and phenylhydroquinone (PHQ) had no effects at the same level. Histopathologically, a single intravesical injection of 0.1% PBQ induced epithelial hyperplasia of the bladder epithelium on day 5, but PHQ and OPP did not induce it. Feeding studies with OPP-Na were also performed to examine the correlation between urinary PBQ levels and DNA damage in bladder epithelium. Slight DNA damage was observed in males given 1.0 and 2.0% OPP-Na in the diet for 3-5 months. The damage was dependent upon the dietary levels of OPP-Na. The amounts of OPP, PHQ and PBQ in urine were well correlated with the dietary levels of OPP-Na for male rats. The amounts of OPP, PHQ and PBQ were greater in male rats than in females given 2.0% OPP-Na diet for 5 months. The urinary pH of males was slightly higher than that of females. Since 0.4% sodium bicarbonate did not cause DNA damage in the in-situ study, the urinary alkalinity may not affect the initiation steps of urinary carcinogenesis by OPP-Na. The present results indicate that the metabolite PBQ is the reactive species for the initiation steps of bladder tumors induced by OPP-Na and OPP.

Animals↗
PubMed1979

Studies on lactic dehydrogenase of patients with urinary bladder tumors. I. Urinary lactic dehydrogenase.

Urinary lactic dehydrogenase (LDH) activity and isozyme pattern were investigated in 38 patients with bladder tumors of various stages and grades and in 10 healthy persons. Urinary LDH activity was markedly elevated and directly correlated with histologic stage and grade of tumors. The urinary LDH isozyme pattern differed significantly from that of normal urine even in early and well-differentiated tumor cases. LDH4 and LDH5 became more prominent as the degree of the histologic stage and grade of the tumor increased. In the patients with tumors more advanced than stage T2, LDH4 and LDH5 were greater than LDH1 plus LDH2, the reverse of what is found in normal urine. As analogous result was obtained in patients with tumors of grade II or higher. No appreciable difference was found in the LDH isozyme pattern of patients with single or multiple tumors although the total activity was greater with multiple tumors. A comparison between LDH isozyme pattern in urine and in tumor tissue was evaluated in 26 patients with a good correlation (r = 0.40, P less than 0.05). Comparison of the results with urine LDH and urine cytology was attempted for each stage and grade. In 5 of 16 cases having negative urine cytology, a positive isozyme index was present and 10 of 13 cases having positive urine cytology had a positive isozyme index. These data suggest that evaluation of urinary LDH combined with urinary cytology might be of value in the diagnosis of bladder tumors and for following patients who have had bladder tumors.

Adult↗
PubMed1987

Experimental model for investigating bladder carcinogen metabolism using the isolated rat urinary bladder.

The capacity of the isolated rat urinary bladder to metabolize chemical carcinogens was studied. Under our experimental conditions, the bladder carcinogen N-nitrosobutyl-(4-hydroxybutyl)amine (NBHBA) was oxidized to N-nitrosobutyl(3-carboxypropyl)amine (NBCPA). A time-dependent increase in the amount of NBCPA formed and a simultaneous disappearance of NBHBA indicated that the bladder can metabolize NBHBA to the metabolite considered to be responsible for tumour induction in the urinary bladder of laboratory animals. After 15, 30, 60 and 120 min, the percentages of NBCPA formed were 10%, 21%, 35% and 61%, respectively, and 59%, 49%, 36% and 25% of NBHBA remained unchanged. When N-nitrosodi-n-butylamine (NDBA) was introduced into the isolated urinary bladder and incubated for 120 min, its oxidized metabolites NBHBA and NBCPA were formed, in amounts of 0.13% and 0.06% of the substrate added.

Animals↗
PubMed1986

Muscarinic receptor density in the rat urinary bladder after denervation, hypertrophy and urinary diversion.

Parasympathetic denervation of the urinary bladder results in supersensitivity to muscarinic agonists and in bladder hypertrophy. In the present study, the effects of denervation on the muscarinic receptors in the rat bladder were investigated, using a receptor binding technique with (-)3H-QNB as radioligand. The density of muscarinic receptors was increased in denervated, hypertrophied bladders but it was decreased, below that in control bladders, when the development of hypertrophy was prevented by urinary diversion. A decreased receptor density was also found in innervated bladders after urinary diversion, whereas the receptor density was unaffected by hypertrophy alone. Competition experiments with methacholine revealed no changes in the agonist binding properties of the receptors. When the present data are combined with those in previous functional studies, it seems unlikely that the muscarinic receptors in the bladder are involved in the development of supersensitivity. It is suggested that the density of muscarinic receptors in the bladder may be related to the bladder function.

Animals↗
PubMed1983

The influence of phenacetin or mechanical perforation on the development of renal pelvic and urinary bladder tumors in FANFT-induced urinary tract carcinogenesis.

The influence of 0.535% phenacetin in the diet or mechanical perforation of the renal pelvis and urinary bladder of male Sprague-Dawley rats in FANFT-induced urinary tract carcinogenesis was studied. The 151 rats were divided into 5 experimental and one control group. The rats were followed for up to 80 weeks. FANFT administered at 0.2% in the diet for 11 weeks resulted in a high incidence of urinary tract tumors particularly of the renal pelvis. Similar results were obtained by administration of 0.2% FANFT for 6 weeks followed by 0.535% phenacetin while FANFT for 6 weeks preceded or followed by mechanical perforation of the renal pelvis resulted in a significantly lower incidence of renal pelvic tumors. Phenacetin appeared to enhance the development of renal pelvic tumors in FANFT-induced urinary tract carcinogenesis. In contrast no effect of phenacetin on the urinary bladder could be detected.

Animals↗
PubMed1982

Effects of adrenergic drugs on miniature contractions of isolated dog urinary bladder.

Isolated dog urinary bladder showed spontaneous miniature contractions under a steady state. In dome preparations, norepinephrine and isoproterenol decreased the frequency of miniature contractions, while epinephrine produced biphasic responses on it; increase by low concentration and decrease by high concentrations. The height of miniature contractions was decreased by these drugs. In trigone preparations, norepinephrine and epinephrine increased the frequency of miniature contractions, while isoproterenol decreased it. These drugs decreased the height of miniature contractions. In both preparations, phentolamine enhanced the decreases in frequency and height by norepinephrine, epinephrine and isoproterenol, while propranolol depressed or reversed them. A computer analysis showed positive and significant correlations between changes in tension development of bladder and frequency and height of miniature contractions. Results indicate that miniature contractions in both dome and trigone of isolated dog urinary bladder are increased by activation of alpha-adrenoceptors and decreased by activation of beta-adrenoceptors.

Animals↗
PubMed2003

Phospholipase C inhibitors suppress spontaneous mechanical activity of guinea pig urinary bladder smooth muscle.

Urinary bladder smooth muscle (UBSM) exhibits spontaneous rhythmic contraction. This spontaneous mechanical activity is generated in the presence of neuronal blockade and thus is myogenic in origin. The spontaneous myogenic contraction of UBSM may be the fundamental determinant of the physiological functions of the urinary bladder to store and excrete urine. Although the mechanisms by which UBSM generates spontaneous contraction have not been completely ascertained, its induction has been suggested to be intimately associated with smooth muscle cell action potentials to enhance extracellular Ca(2+) influx through voltage-gated L-type Ca(2+) channels. However, the alteration of membrane electrical activity does not seem to be the exclusive trigger mechanism for the generation of the spontaneous contraction. In the present study, we show that spontaneous mechanical activity of guinea pig UBSM is substantially diminished by an inhibitor of phospholipase C (PLC), U-73122, but is not affected by its inactive form, U-73343. Significant attenuation of the mechanical activity can be also obtained with another PLC inhibitor 2-nitro-4-carboxyphenyl-N,N-diphenylcarbamate. Our present findings suggest a significant role for the activation of PLC and subsequent inositol 1,4,5-trisphosphate-induced Ca(2+) release mechanism as an alternative triggering system for inducing spontaneous mechanical activity of UBSM. The present results support the idea that the action potential is not the sole pacemaker mechanism by which spontaneous contraction is induced in UBSM.

Animals↗
PubMed1987

Biotransformation of aromatic amines to DNA-damaging products by urinary bladder organ cultures.

Urinary bladder is a target tissue for aromatic amine carcinogens. The intrinsic capacity of this tissue to form DNA-damaging products was investigated in explant cultures of bladder isolated from New Zealand white rabbits. DNA repair, measured by autoradiography, was used as the indicator of DNA damage. DNA repair was induced by 2-aminofluorene (2-AF) and its acetylated derivatives 2-acetyl-aminofluorene and N-hydroxy-2-acetylaminofluorene. A positive response was observed with benzidine (BZD), but no repair was seen in cultures exposed to monoacetyl BZD or diacetyl BZD. These results indicate that rabbit urinary bladder has the ability to biotransform aromatic amines to DNA-damaging products and has the capacity to repair damaged DNA. Unlike liver, where activation of BZD seems to require N-acetylation, acetylated BZD in the bladder appeared to be a detoxification product. The lack of damage by acetylated BZD is consistent with activation of BZD in bladder by prostaglandin synthetase-mediated pathways.

2-Acetylaminofluorene↗