Bladder Outlet Obstruction Rats Research Articles

The Role of Muscarinic Receptor Subtype on Detrusor Overactivity induced by Bladder Outlet Obstruction in Rats

The Role of Muscarinic Receptor Subtype on Detrusor Overactivity induced by Bladder Outlet Obstruction in Rats

Changes in Corpus Cavernosum after Partial Bladder Outlet Obstruction in Rat

Purpose: Abnormalities of the relaxation and contraction of the corpus cavernosum can lead to erectile dysfunction. Therefore, we induced a partial bladder outlet obstruction(PBOO) in male rats, and investigated the mechanisms of penile dysfunction with endothelial nitric oxide synthase(eNOS), vascular endothelial growth factor(VEGF), endothelin-1(ET-1), and apoptosis of peri-vascular smooth muscle and connective tissue cells in the corpus cavernosum. Materials and Methods: PBOO was induced in 13 Sprague-Dawley rats by placing a 25 gauge needle sheath around the urethra, then ligating the bladder neck with a 3-0 suture. Three week after surgery, distal penile tissues were dissected for immunohistochemical staining, immunoblotting, and TUNEL staining. Results: The expression of eNOS and VEGF were significantly decreased, whereas the expression of ET-1 and apoptosis of perivascular smooth muscle and connective tissue cells were significantly increased in the corpus cavernosum. Conclusions: The significant increase of ET-1 and apoptosis along with decreased eNOS and VEGF could mediate erectile dysfunction.

Nicorandil, a Potassium Channel Opener and Nitric Oxide Donor, Improves the Frequent Urination without Changing the Blood Pressure in Rats with Partial Bladder Outlet Obstruction

It was studied to determine if nicorandil can improve frequent urination in rats with partial bladder outlet obstruction (BOO) without changing the blood pressure. Voiding behavior was observed 6 to 8 d after obstruction in female rats with BOO that loaded 30 ml/kg of water. A drug was administered orally. Changes in systemic blood pressure and heart rate were studied in conscious BOO rats using the tail cuff method. The voiding frequency was increased and the average voided volume was decreased in BOO rats compared with normal rats. Nicorandil (1 mg/kg), cromakalim (0.1 mg/kg) and isosorbide dinitrate (ISDN; 1000 mg/kg) decreased voiding frequency significantly in BOO rats. Nicorandil also increased the average voided volume significantly. Although cromakalim and ISDN at doses effective at decreasing voiding frequency caused blood pressure to drop, nicorandil at an effective dose did not affect blood pressure and heart rate. Nicorandil improved frequent urination without changing the blood pressure. These results suggested that a hybrid of a K(ATP) channel opener and nitric oxide donor, nicorandil was bladder-selective compared with vasculature in BOO rats.

Change in acetylcholine release from rat bladder with partial outlet obstruction

To investigate changes in acetylcholine release from the bladder of rats with partial bladder outlet obstruction (BOO), as partial BOO leads to hypertrophy and an alteration in the contractions of the detrusor smooth muscle, and acetylcholine plays an important role in urinary bladder contractions but there is little available information on acetylcholine release after BOO. Partial BOO was induced in adult female rats by ligating the proximal urethra over a 1 mm angiocatheter; sham-operated rats served as controls. The rats were killed 2 weeks, 3 and 6 months after induction of BOO. We investigated the contractions induced by carbachol, KCl (80 mm), ATP and electrical-field stimulation (EFS, 2.5-40 Hz), and collected the dialysate obtained from a microdialysis probe inserted into the muscle strips during EFS, and measured the amount of acetylcholine in the dialysate fraction by high-performance liquid chromatography with electro-chemical detection. S-100 immunohistochemical staining of the bladder preparations was used for histological examination in BOO and control rats. The bladder weight gradually increased after BOO. There were no significant changes in KCl-induced contractions throughout the experimental period in either group. There were no significant changes in carbachol-induced contractions until 3 months after BOO but there was a significant reduction at 6 months. ATP-induced contractions were significantly increased 2 weeks and 3 months after BOO. EFS-induced contractions were gradually reduced after BOO. Acetylcholine release from the bladder strips was not significantly different between the groups until 2 weeks after BOO. However, acetylcholine release in BOO rats was significantly decreased 3-6 months after BOO, being significantly lower than that of the control rats. In the histological study, the number of nerve fibres in the BOO rats was significantly lower than in the control rats. We suggest that the prolonged BOO caused a decrease in EFS-induced acetylcholine release and the number of nerves in the rat urinary bladder, which might contribute to bladder underactivity in BOO.

Inhibitory effects of nicorandil, a KATP channel opener and a nitric oxide donor, on overactive bladder in animal models

To investigate the effects of nicorandil, an ATP-sensitive potassium (K(ATP)) channel opener with a nitric oxide (NO) donor property, on overactive bladder (OAB) in animal models. Nicorandil is currently used clinically to treat ischaemic heart disease. Three animal OAB models were used: (i) C-fibre mediated bladder overactivity by infusion of a low concentration of acetic acid (AA) into the bladder in female Wistar rats; (ii) bladder outlet obstruction (BOO) created by partial urethral obstruction in female Wistar rats; and (iii) neuronal NO synthase (nNOS) knockout (KO) mice with urinary frequency. The effects of nicorandil and KRN2391, both of which act as K(ATP) channel openers and NO donors, on the OAB models were examined. Cystometry showed that intravesical instillation of nicorandil and KRN2391 successfully inhibited OAB induced by intravesical instillation of AA. In the BOO model compared with untreated BOO rats, both nicorandil (1 and 3 mg/kg, orally) and KRN2391 (1 mg/kg, orally) significantly reduced the voiding frequency. Compared with wild-type mice, nNOS KO mice had urinary frequency with no change in the total urine volume. Nicorandil (3 mg/kg, orally) and KRN2391 (1 mg/kg, orally) significantly reduced the voiding frequency in nNOS KO mice. Our in vivo results show that nicorandil, a K(ATP) channel opener with a NO donor property, can suppress OAB from both neurogenic and myogenic causes. Nicorandil appears to be a promising candidate for clinical use in patients with OAB.

Suppression of detrusor overactivity in rats with bladder outlet obstruction by a type 4 phosphodiesterase inhibitor

To investigate the effects of a selective type 4 cyclic nucleotide phosphodiesterase (PDE4) inhibitor, IC486051, on bladder activity in normal rats and those with and bladder outlet obstruction (BOO), as inhibition of PDE4 leads to elevation of intracellular cAMP levels and relaxation of smooth muscle. BOO was induced in female Sprague-Dawley rats by tying a silk ligature around the urethra. At 4 or 6 weeks after inducing BOO, conscious rats were assessed by cystometry with the urethral ligature intact. In unobstructed rats, blood pressure was also measured. In unobstructed rats, IC486051 (0.1 mg/kg intravenously) produced no significant changes in cystometric variables, while at a dose of 0.5 mg/kg maximum voiding pressure was reduced by 34%. At both doses, there was a small, transient increase in blood pressure. In both 4- and 6-week BOO rats IC486051 dose-dependently decreased the number and amplitude of non-voiding bladder contractions by up to 80%, relative to pre-treatment values. At doses of 0.1 and 0.5 mg/kg IC486051 had no significant effect on voiding variables. In the 4-week BOO rats, a dose of 1.0 mg/kg decreased bladder capacity, voided volume and residual volume by 21%, 32% and 18%, respectively. In 6-week BOO rats, a dose of 1.0 mg/kg decreased maximal voiding pressure by 17% and pressure threshold for voiding by 28%. In both groups of rats with BOO, voiding efficiency was unchanged. A selective PDE4 inhibitor can effectively suppress detrusor overactivity in rats with BOO, at doses that have no effect on voiding bladder contractions. Thus, selective PDE4 inhibitors should be considered for the treatment of overactive bladder in patients with BOO.

Urodynamics and bladder muscarinic receptors in rats with cerebral infarction and bladder outlet obstruction

We characterized muscarinic receptor binding and urodynamic parameters in rats with cerebral infarction and chronic bladder outlet obstruction as models of detrusor overactivity. Bladder weight showed little significant difference between the cerebral-infarcted and sham rats, but the bladder weight was about three times greater in the bladder outlet-obstructed rats. Bladder capacity and voided volume were significantly lower (36.7 and 55.1%, respectively) in the cerebral-infarcted than in the sham rats. Involuntary contractions before micturition were seen in the bladder outlet-obstructed rats but not in sham rats. The bladder outlet-obstructed rats showed significant increases (2.65 and 2.57 times, respectively) in bladder capacity and voided volume, compared with those in sham rats. Bmax values for specific [N-methyl-3H]scopolamine ([3H]NMS) binding in the bladder were significantly (34%) increased in the cerebral-infarcted rats compared with sham rats, whereas Kd was unaffected by infarction. On the other hand, there was little significant change in Kd and Bmax for specific [3H]NMS binding in the bladder-obstructed rats compared with sham rats. In conclusion, the present study shows that cerebral infarction but not bladder outlet obstruction in rats causes up-regulation of bladder muscarinic receptors, and that such regulation of bladder muscarinic receptors may be at least partly associated with the symptoms of detrusor overactivity subsequent to cerebral infarction.

The Effect of Muscarinic Receptor Subtype Antagonists on Detrusor Overactivity Induced by Bladder Outlet Obstruction in Rats

Purpose: We studied the role of the muscarinic receptor subtype on the urothelium and detrusor activity in rats with detrusor overactivity induced by bladder outlet obstruction (BOO). Materials and Methods: Forty Sprague-Dawley rats were used for this study. They were divided into 15 controls and 25 experimental rats. Partial BOO was induced for 3 weeks and a sham operation was performed on the control group animals. A cystometrogram (CMG) was performed in 20 BOO and 10 control rats. During the CMG, M2 selective muscarinic receptor antagonist (methoctramine) and nonselective muscarinic receptor antagonist (tolterodine) drugs were administrated intravesically. The contraction intervals and pressure were evaluated. Bladder muscle strips were prepared from five BOO and five control rats. The contractile responses were evaluated at 2-, 4-, 8-, 16-, and 32Hz field stimulation in the control and BOO groups and after administration of the methoctramine and tolterodine. Results: The results of the CMG showed that the rats in the BOO group had a decreased contraction interval and increased contraction pressure compared to the control group (p＜0.05). The contraction intervals were increased after intravesical administration of methoctramine and tolterodine compared to the BOO group (p＜0.05). However, the contraction pressures were similar among the methoctramine, tolterodine and BOO groups. For the muscle strip study, the BOO group demonstrated increased contractile responses compared to the control group (p＜0.05). However, the contractile responses were decreased after administration of methoctramine (only in 32Hz) and tolterodine (p＜0.05). Conclusions: The results of this study showed that detrusor overactivity induced by BOO in rats is primarily mediated by M3 muscarinic receptors in the detrusor muscle, and by M2 and M3 muscarinic receptors in the

Effects of Rho Kinase Inhibitor on Detrusor Overactivity after Bladder Outlet Obstruction in Rats

Results: The bladder weights of the PBOO group were significantly increased compared with the control group (p＜0.05). Significant increases in the voiding frequency and PP, but a significant decrease in the ICI was observed in the PBOO group compared to the control group on the CMG (p＜0.05). The voiding frequency of the PBOO group was significantly decreased after Rho kinase inhibitor treatment (p＜0.05). The Rho kinase inhibitor treated group showed a decrease in the PP and an increase in the ICI compared to the PBOO group. The IHC showed a higher RhoA protein expression in the bladder tissues of the PBOO group. Conclusions: H-1152, a specific inhibitor of Rho kinase, attenuates the PBOO-related detrusor overactivity in a rat model. The Rho kinase inhibitor appears to be a novel strategy for the management of bladder

Effect of short‐term outlet obstruction on rat bladder nerve density and contractility

1 The present study was designed to investigate the relationship between innervation density and contractile responses to field stimulation and exogenous agonists at early time points after induction of bladder outlet obstruction (BOO) in rats. 2 When compared with sham-operated animals, 1, 3 and 7 days of BOO were associated with a 75%, 80% and 90% increase of bladder weight. Field stimulation caused a frequency-dependent increase in force of contraction. The force of contraction was reduced at each frequency in BOO rats with the greatest decrease after 1 day and a gradual but incomplete recovery thereafter. In contrast, contractile responses to ATP, carbachol and KCl were markedly reduced after 1 day of BOO and fully recovered after 7 days. The neurofilament staining was not altered by 1 day of BOO, but gradually decreased with increasing duration of BOO reaching the lowest levels after 7 days. 3 We conclude that impaired cellular contractility seems to underlie the early reductions of field stimulation-induced contraction, possibly reflecting surgical trauma of the tissue. However, at later time points a reduced nerve density, possibly reflecting a partial denervation, appears to be the main reason for impaired contractile response to field stimulation.

Characterization and Functional Role of Androgen-Dependent PDE5 Activity in the Bladder

Benign prostate hyperplasia is the most common disease in the aging male, often comorbid with erectile dysfunction. Phosphodiesterase type 5 (PDE5) inhibitors (sildenafil, tadalafil, and vardenafil) decrease lower urinary tract symptoms in patients with erectile dysfunction and BPH. We studied PDE5 expression and activity in the human bladder and PDE5i effects both in vitro (human and rat) and in vivo (rat). PDE5 is highly expressed in rat and human bladder and immunolocalized in vascular endothelium and muscle fibers. Sildenafil, tadalafil, and vardenafil blocked 70% of the total cGMP-catabolizing activity; vardenafil was the most potent (IC(50) = 0.3 nm). In human bladder cells and in rat strips, a PDE-resistant cGMP analog, SP-8-Br-PET-cGMPS, induced, respectively, a consistent antiproliferative and relaxant effect. In contrast, the nitric oxide donor sodium nitroprusside (SNP) was almost ineffective. However, blocking PDE5 with vardenafil increased SNP antiproliferative and relaxant activity up to the level observed with SP-8-Br-PET-cGMPS. We also found that castration decreased, and T supplementation restored, PDE5 gene expression in rat bladder. Accordingly, bladder strips from castrated rats were more sensitive to SNP-induced relaxation than strips from control or T-replaced rats, whereas in the presence of vardenafil, all groups showed the same SNP sensitivity. To discover whether vardenafil affects bladder activity in vivo, the rat bladder outlet obstruction model was used. Chronic treatment with 10 mg/kg.d vardenafil significantly reduced nonvoiding contractions (47%, P < 0.05 vs. placebo) up to tamsulosin level (51%). Overall, these results demonstrate that PDE5 regulates bladder smooth muscle tone, strongly limiting the nitric oxide/cGMP signaling, and that vardenafil, by blocking PDE5, may be a possible therapeutic option for bladder dysfunction by ameliorating irritative lower urinary tract symptoms.

Participation of endogenous endothelin and ETA receptor in premicturition contractions in rats with bladder outlet obstruction

A relationship between endogenous endothelins and bladder overactivity has recently been suggested, but the related endothelin receptor subtype has not been identified. Here, to evaluate the involvement of endothelin-1 and its receptors in bladder overactivity, we investigated endothelin-1 levels and the expression of its receptors in the bladder of rats with bladder outlet obstruction (BOO), a model for bladder overactivity. We also investigated the effects of a selective endothelin ET(A) receptor antagonist, (E)-N-[6-methoxy-5-(2-methoxyphenoxy)[2,2'-bipyrimidin]-4-yl]-2-phenylethenesulfonamide monopotassium salt (YM598), on bladder functions in conscious BOO rats. Partial obstruction of the urethra led to a progressive increase in bladder weight from weeks 1 to 6. Binding assays performed using plasma membranes prepared from these bladders to estimate endothelin receptor density from the maximum [(125)I]endothelin-1 binding showed increased endothelin receptor density (about double) at 1, 2, and 6 weeks after the operation in the BOO bladder. The densities of endothelin ET(A) receptors in the bladder of sham-operated and BOO rats at 2 weeks after operation were about 3.5 and 5 times those of endothelin ET(B) receptors respectively. Furthermore, the endothelin-1 level was also increased in the BOO bladder. Two weeks after operation, BOO rats showed an increase in maximum bladder capacity and micturition volume and the generation of premicturition contractions. The frequency of premicturition contractions was dose-dependently reduced by YM598 (0.1-3 mg/kg, i.v.) without any effect on other voiding parameters in BOO rats. These data suggest that endothelin-1 and endothelin ET(A) receptors might be involved in the generation of premicturition contractions in BOO rats, and that endothelin ET(A) receptor antagonists such as YM598 may have ameliorating effects in patients with bladder overactivity associated with BOO.

1455: Alfuzosin Reverses Bladder Hypertrophy Induced by Bladder Outlet Obstruction in Rats

1455: Alfuzosin Reverses Bladder Hypertrophy Induced by Bladder Outlet Obstruction in Rats

Cystometric evaluation of partial urinary bladder outlet obstruction model in conscious rats

Urinary frequency and urgency in benign prostatic hyperplasia (BPH) are associated with involuntary detrusor contractions. Animals with partial bladder outlet obstruction (BOO) exhibit detrusor instability showing non-micturition contractions (NMC) on cystometrogram (CMG). We investigated the conscious CMG and natural voidings (NV) of rats with BOO. The effect of 5-HT1A antagonist WAY100635 (WAY) on NMC was also evaluated in the BOO rats. The proximal urethra was loosely ligated. NV and CMG were measured 2–6 weeks post BOO. The ligature was removed and the bladder was cannulated 2 days prior to CMG. The bladder weight of BOO was increased significantly 3–6 weeks post BOO. [Bladder weight (g): BOO 0.53±0.04 (n=18), sham 0.18±0.01 (n=16)]. Histopathological abnormalities were seen in the bladders and kidneys in BOO rats. No NV difference was observed between BOO and sham. The void pressure (VP), void interval (VI) and void volume (VV) were not significantly different within 3–6 week BOO rats, however the VI and VV were increased and significantly different from sham rats. [VI (min): BOO 13.8±0.8, sham 6.16±0.4 (p<0.01); VV (ml): BOO 2.7±0.3, sham 1.3±0.1 (p<0.01)]. NMC was exhibited in 9 of 17 BOO rats, but not in sham controls. WAY (0.1 mg/kg, iv) significantly inhibited NMC. [Inhibition time (min): WAY 7.4±3.1, veh 0±0 (n=4, p<0.05); Amplitude inhibition (mmHg): WAY −11.3±2.9, veh −0.5±1.2; (n=4, p<0.05)]. These results indicate that BOO could induce increased bladder capacity and void interval and NMC in conscious rats. WAY100635 produced inhibitory effect on NMC, suggesting that 5-HT1A antagonist may inhibit detrusor instability associated with outlet obstruction in BPH.

1204: Relationship between Acetylcholine and ATP Releases and Bladder Smooth Muscles Function in Partial Bladder Outlet Obstruction in Rats

You have accessJournal of UrologyDiscussed Poster, Tuesday, May 24, 2005, 1:00 - 5:00 pm1 Apr 20051204: Relationship between Acetylcholine and ATP Releases and Bladder Smooth Muscles Function in Partial Bladder Outlet Obstruction in Rats Koichi Masunaga, Masaki Yoshida, Akito Inadome, Masayuki Otani, Yutaka Sugiyama, Yo Satoji, Yoshihiro Maeda, and Shoichi Ueda Koichi MasunagaKoichi Masunaga More articles by this author , Masaki YoshidaMasaki Yoshida More articles by this author , Akito InadomeAkito Inadome More articles by this author , Masayuki OtaniMasayuki Otani More articles by this author , Yutaka SugiyamaYutaka Sugiyama More articles by this author , Yo SatojiYo Satoji More articles by this author , Yoshihiro MaedaYoshihiro Maeda More articles by this author , and Shoichi UedaShoichi Ueda More articles by this author View All Author Informationhttps://doi.org/10.1016/S0022-5347(18)35349-7AboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissionsReprints ShareFacebookLinked InTwitterEmail "1204: Relationship between Acetylcholine and ATP Releases and Bladder Smooth Muscles Function in Partial Bladder Outlet Obstruction in Rats." The Journal of Urology, 173(4S), pp. 326–327 © 2016 by American Urological AssociationFiguresReferencesRelatedDetails Volume 173Issue 4SApril 2005Page: 326-327 Advertisement Copyright & Permissions© 2016 by American Urological AssociationMetricsAuthor Information Koichi Masunaga More articles by this author Masaki Yoshida More articles by this author Akito Inadome More articles by this author Masayuki Otani More articles by this author Yutaka Sugiyama More articles by this author Yo Satoji More articles by this author Yoshihiro Maeda More articles by this author Shoichi Ueda More articles by this author Expand All Advertisement PDF downloadLoading ...

1201: Changes of Connexin43-Derived Gap Junctions in the Bladder and Glycine in the Lumbosacral Cord after Partial Bladder Outlet Obstruction in Rats

You have accessJournal of UrologyDiscussed Poster, Tuesday, May 24, 2005, 1:00 - 5:00 pm1 Apr 20051201: Changes of Connexin43-Derived Gap Junctions in the Bladder and Glycine in the Lumbosacral Cord after Partial Bladder Outlet Obstruction in Rats Minoru Miyazato, Kimio Sugaya, Saori Nishijima, Atsushi Uchida, Makoto Morozumi, and Yoshihide Ogawa Minoru MiyazatoMinoru Miyazato More articles by this author , Kimio SugayaKimio Sugaya More articles by this author , Saori NishijimaSaori Nishijima More articles by this author , Atsushi UchidaAtsushi Uchida More articles by this author , Makoto MorozumiMakoto Morozumi More articles by this author , and Yoshihide OgawaYoshihide Ogawa More articles by this author View All Author Informationhttps://doi.org/10.1016/S0022-5347(18)35346-1AboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissionsReprints ShareFacebookLinked InTwitterEmail "1201: Changes of Connexin43-Derived Gap Junctions in the Bladder and Glycine in the Lumbosacral Cord after Partial Bladder Outlet Obstruction in Rats." The Journal of Urology, 173(4S), p. 326 © 2016 by American Urological AssociationFiguresReferencesRelatedDetails Volume 173Issue 4SApril 2005Page: 326 Advertisement Copyright & Permissions© 2016 by American Urological AssociationMetricsAuthor Information Minoru Miyazato More articles by this author Kimio Sugaya More articles by this author Saori Nishijima More articles by this author Atsushi Uchida More articles by this author Makoto Morozumi More articles by this author Yoshihide Ogawa More articles by this author Expand All Advertisement Loading ...

816Effect of angiotensin-converting enzyme inhibitor on connexin expression after bladder outlet obstruction in rats

816Effect of angiotensin-converting enzyme inhibitor on connexin expression after bladder outlet obstruction in rats

The restorative effect of a selective cyclooxygenase‐2 inhibitor on urothelial cell–cell interactions after partial bladder outlet obstruction in rats

To determine the changes in cyclooxygenase-2 (COX-2), E-cadherin and alpha-catenin expression after partial bladder outlet obstruction (PBOO), and whether a selective COX-2 inhibitor (celecoxib) might inhibit COX-2 expression and have beneficial effects on urothelial cell-to-cell interactions in rats subjected to PBOO. Thirty-six male rats were divided into six equal groups; celecoxib was administered after creating PBOO for 1 and 4 weeks in groups 1 and 2, respectively. Two further obstructed groups (3 and 4, PBOO for 1 and 4 weeks, respectively) received no treatment. Sham-operated animals served as controls (group 5 and 6, assessed at 1 and 4 weeks, respectively). After 1 and 4 weeks of PBOO or a sham procedure the bladder weight was recorded before sampling the bladder for Western blotting and immunohistological analysis, to assess the expressions of COX-2 and adherens proteins, E-cadherin and alpha-catenin. Urothelial cell-to-cell interactions were evaluated using electron microscopy. The bladder mass increased rapidly during the first 7 days after PBOO in groups 1-4 compared with 5 and 6 (P < 0.05). While the bladder mass then continued to increase for the next 21 days in group 4, it was constant in group 2 (P < 0.001). Immunohistochemical staining and Western blotting analyses showed that E-cadherin and alpha-catenin expression were reversibly decreased in rats with PBOO, while COX-2 protein expression was up-regulated. After giving celecoxib there was a significant decrease in COX-2 expression and a restoration of intercellular adherens junctions and desmosomes, as assessed on electron microscopy and expression of adherens proteins combined. The increase in COX-2 expression attributable to hypoxia and the tensile strength of bladder wall was attenuated by celecoxib. Selective COX-2 inhibitors have important restorative effects on intercellular adherens junctions and desmosomes in PBOO.

Nerve growth factor and vanilloid receptor expression, and detrusor instability, after relieving bladder outlet obstruction in rats.

To investigate mRNA expression for nerve growth factor (NGF) and vanilloid receptor TRPV1 in the bladder after relieving bladder outlet obstruction (BOO), and to correlate changes with functional changes of the bladder. Temporary BOO was induced by partial urethral ligation in 40 male Wistar rats. After 3 weeks the obstruction was removed and the rats assessed by cystometry 3 weeks later. The bladder body of each rat was then removed, and NGF and TRPV1 mRNA expression measured by the reverse transcription-polymerase chain reaction. Fifteen sham-operated rats served as controls. Based on the cystometry, 10 of the 40 experimental rats were judged to have an unstable bladder, and the remaining 30 to have normal bladder function. The mean bladder weight in the normal and unstable groups was higher than in the control group, and there was no significant difference between the normal and unstable groups. The bladder contraction pressure was similar in the three groups but the mean contraction interval was markedly shorter in the unstable than in the control and normal groups (P < 0.05). The mRNA expressions of NGF and TRPV1 were higher in the unstable than in the control and normal groups. NGF and TRPV1 were apparently increased in unstable bladder tissue after relieving BOO; these changes may be related to irritative symptoms after correcting BOO.

Evidence of Gap Junctions in the Stable Nonobstructed Human Bladder

Evidence of Gap Junctions in the Stable Nonobstructed Human Bladder