α1 -Blocker inhibits non-voiding contractions and decreases the level of intravesical prostaglandin E2 in rats with partial bladder outlet obstruction.

OBJECTIVES: To elucidate the mechanism of action of the α1 -blocker, naftopidil, in partial bladder outlet obstruction animals, by studying non-voiding contractions, and the levels of mediators were measured with resiniferatoxin treatment. METHODS: A total of 35 female Wistar rats were randomly divided into a sham or bladder outlet obstruction group, and rats in each group were given vehicle or resiniferatoxin. Incomplete urethral ligation was applied to the bladder outlet obstruction group. After cystometry, the intravesical level of prostaglandin E2 and adenosine 5'-triphosphate was measured in the instilled perfusate collected. Naftopidil was given at the time of cystometry. RESULTS: In bladder outlet obstruction rats, non-voiding contractions, bladder capacity, and the intravesical levels of prostaglandin E2 and adenosine 5'-triphosphate were markedly increased compared with sham rats. Naftopidil decreased non-voiding contractions, enlarged the bladder capacity, and decreased the intravesical levels of prostaglandin E2 and adenosine 5'-triphosphate. Resiniferatoxin enhanced non-voiding contractions. The effects of naftopidil on non-voiding contractions and the intravesical level of prostaglandin E2 , but not adenosine 5'-triphosphate, were tolerant to resiniferatoxin. CONCLUSIONS: In bladder outlet obstruction rats, one cause of generation of non-voiding contractions might be bladder wall distension, but not transient receptor potential cation channel V1. The increase in intravesical prostaglandin E2 might also be associated with the generation of non-voiding contractions. Naftopidil inhibits the increase in non-voiding contractions and decreases the intravesical level of prostaglandin E2 , which are independent of transient receptor potential cation channel V1.

Nerve growth factor release from the urothelium increases via activation of bladder C-fiber in rats with cerebral infarction.

AIMS: There are some reports that bladder C-fibers are partially involved in detrusor overactivity in patients with brain lesions. We investigated the contribution of bladder C-fiber to decreased bladder capacity in rats with cerebral infarction. METHODS: Cerebral infarction was induced under halothane anesthesia by left middle cerebral artery occlusion with 4-0 nylon thread in female Sprague-Dawley rats. Intramural amounts of ATP and prostaglandin E2 , in vivo and in vitro ATP, NGF, and prostaglandin E2 release from the distended bladder urothelium, and changes in mRNA expressions of sensor molecules and receptors were monitored 6 h after the occlusion. Cystometry was performed in rats with or without resiniferatoxin pretreatment. RESULTS: Overexpression of sensor molecule, transient receptor potential vanilloid-type channel 1, acid-sensing ion channel 2, purinergic receptors P2X3 , and M2 /M3 muscarinic receptors was found in the bladder. These changes were accompanied by increases in ATP and NGF release from the urothelium. In contrast, when bladder C-fibers were desensitized by resiniferatoxin, no increase in NGF release from the urothelium was found either in vivo or in vitro. There was no difference in the percentage decrease in bladder capacity between cerebral infarction rats pretreated with resiniferatoxin and cerebral infarction rats without pretreatment. CONCLUSIONS: Results indicate that expression of sensor molecules in the bladder is altered by distant infarction in the brain. ATP and NGF release from the urothelium also increased. NGF release was related to activation of bladder C-fibers. Bladder C-fibers might not contribute much to decreased bladder capacity caused by cerebral infarction.

Nocturnal Polyuria and Hypertension in Patients with Lifestyle Related Diseases and Overactive Bladder.

PURPOSE: The objective of this multicenter cross-sectional study was to investigate the relationship of nocturnal polyuria in patients with common lifestyle related diseases and overactive bladder, with special attention to hypertension. MATERIALS AND METHODS: After baseline assessment, patients recorded 24-hour urinary frequency/volume, blood pressure and heart rate for 3 days. They were stratified into 4 groups based on mean blood pressure, including no hypertension, and controllable, untreated and uncontrolled hypertension, respectively. RESULTS: The 2,353 eligible patients, who had urinary urgency once or more per week and 1 or more nocturnal toilet visits, were enrolled from 543 sites in Japan. Of these patients complete data, including the 24-hour frequency volume chart, were collected from 1,271. Multivariable analyses showed a statistically significant association of nocturnal polyuria with increasing age (OR 1.04, 95% CI 1.02-1.05, p <0.001) and gender (women vs men OR 0.75, 95% CI 0.59-0.96, p = 0.02), and for controllable (OR 1.10, 95% CI 0.83-1.460), untreated (OR 2.62, 95% CI 1.55-4.45) and uncontrolled (OR 1.15, 95% CI 0.81-1.62) hypertension vs no hypertension (p = 0.005). However, when assessed separately in men and women, hypertension and heart rate were significantly associated with nocturnal polyuria in women alone (p = 0.01 and 0.03, respectively). Lower urinary tract symptoms suggestive of benign prostatic hyperplasia were significantly associated with nocturnal polyuria in men alone (p <0.001). CONCLUSIONS: The current study demonstrates that nocturnal polyuria was significantly associated with age, male gender, and untreated hypertension in patients with lifestyle related diseases and overactive bladder. The association between hypertension and nocturnal polyuria was significant in women alone.

α1D-Adrenoceptor blockade increases voiding efficiency by improving external urethral sphincter activity in rats with spinal cord injury.

Ideal therapy for lower urinary tract dysfunction in patients with spinal cord injury (SCI) should decrease detrusor overactivity, thereby promoting urine storage at low intravesical pressure and promoting efficient voiding at low pressure by decreasing detrusor-sphincter dyssynergia. Here we investigated blockade of various α-adrenoceptors to determine the subtype that was principally responsible for improving the voiding dysfunction. The effects of the intravenous α-blocker naftopidil, the α-blocker BMY 7378, and the α-blocker silodosin were evaluated using cystometrography and external urethral sphincter-electromyography (EMG) in decerebrated, unanesthetized female Sprague-Dawley rats with chronic SCI following transection at Th8. Parameters measured included the voided volume, residual volume, voiding efficiency, and burst and silent periods on EMG. Compared with values in decerebrated non-SCI rats, EMG of decerebrated SCI rats revealed more prominent tonic activity, significantly shorter periods of bursting activity, and a reduced ratio of the silent to active period during bursting. Compared with the value before drug administration (control), the voiding efficiency was significantly increased by naftopidil (1 and 3 mg/kg) (<0.05 each), and the burst (<0.01 and <0.05, respectively) and silent periods (<0.01 each) on EMG were significantly lengthened. BMY 7378 (1 mg/kg) significantly increased voiding efficiency and lengthened the burst periods (<0.05 each). Silodosin did not affect any parameters. These results suggest that α-blockade reduces the urethral resistance associated with detrusor-sphincter dyssynergia, thus improving voiding efficiency in SCI rats.

Underlying mechanisms of urine storage dysfunction in rats with salt-loading hypertension.

AIMS: Spontaneous hypertensive rats provide a genetic model for exploring the pathogenesis of urine storage dysfunction related to hypertension (HT). In humans, however, HT develops by both genetic and environmental factors including lifestyle factors such as a high-calorie diet, excessive salt intake and stress. We investigated the influence of salt-loading on bladder function and the underlying mechanisms of storage dysfunction related to HT. MAIN METHODS: Six-week-old male Dahl salt-sensitive (DS) and Dahl salt-resistant (DR) rats were fed with a normal or high-salt diet for 12weeks. Micturition parameters were obtained from a metabolic cage. Whole bladders were excised from 18-week-old rats and distended in an organ bath. The releases of adenosine triphosphoric acid (ATP) and prostaglandin E2 (PGE2) from the distended bladder epithelia were measured. Changes in bladder blood flow (BBF) were determined with a laser-speckle-blood-flow imaging system. KEY FINDINGS: An increase in mean blood pressure (BP) was noted only in DS rats after salt-loading. During the inactive (sleeping) period, voided volume per micturition gradually increased in DR rats fed a normal or high-salt diet and normal-diet DS rats, while it did not change in the DS rats fed a high-salt diet. Bladder distension significantly increased ATP and PGE2 release from the urothelium in DS rats fed a high-salt diet. BBF was significantly decreased in high-salt-diet DS rats. SIGNIFICANCE: One mechanism behind the relationship between salt-sensitive HT and urine storage dysfunction may be an increase in ATP and PGE2 release from the urothelium via suppression of BBF.

[A case of metachronal testicular tumor eight years after medical treatment of extragonadal germ cell tumor].

A 22-year-old man was admitted to our hospital complaining of a left cervical mass. Computed tomography (CT) showed multiple enlarged lymph nodes at the left cervical vein and para-aortic areas. Histological examination of a biopsy indicated an embryonal carcinoma. The levels of human ß-chorionic gonadotropin (ß-HCG) and lactic dehydrogenase (LDH) were both elevated. Ultrasonography revealed testicular calcification, but there were no findings on magnetic resonance imaging (MRI). The patient was diagnosed as having an extragonadal germ cell tumor. After four courses of chemotherapy with BEP protocol (bleomycin, etoposide and cisplatin), retroperineal lymph node dissection (RPLND) was performed and there was no involvement of the viable cells in the resected lymph nodes. Eight years after chemotherapy, he noticed an enlargement of his left scrotum without pain. ß-HCG was again elevated. A unilateral high orchiectomy was performed, and histology revealed a seminoma. He was staged as pT1N0M0S0. Six months later he remains disease-free.

Effects of the 5α-reductase inhibitor dutasteride on rat prostate α1A-adrenergic receptor and its mediated contractility.

OBJECTIVE: To clarify the possible interference of the 5α-reductase inhibitor dutasteride with α-adrenergic blockers, whose action is mainly mediated by α1A-adrenergic receptor. METHODS: Male rats were divided into dutasteride and vehicle-treated groups. The drug treatment group was treated with oral dutasteride 0.5 mg/kg/d, and the control group received vehicle only for 2 months. After the 2-month treatment, the rats' ventral prostate weight changes and the testosterone and dihydrotestosterone levels in the serum were measured. In vitro organ-bath studies, real-time polymerase chain reaction, and tissue-segment binding were performed to determine the expression of α1A-adrenergic receptors and its mediated contractility. RESULTS: Dutasteride treatment significantly decreased the rats' ventral prostate weight, increased their testosterone levels, and decreased the dihydrotestosterone levels in their serum. There were no marked changes in the α1A-adrenergic receptor messenger ribonucleic acid expression, relative phenylephrine-induced contractility, or nerve-mediated contractility between the groups. Dutasteride treatment caused no marked changes in the relative binding capacity of α1A-adrenergic receptor, whereas it greatly decreased the total protein expression of this subtype and its mediated maximal contraction in the whole ventral prostate. CONCLUSION: These results suggest that dutasteride does not interfere with α-adrenergic blockers but otherwise has beneficial effects on their actions. Therefore, the long-term administration of the combination of dutasteride with an α-adrenergic blocker might be a better choice for the treatment of lower urinary tract symptoms due to benign prostatic hyperplasia.

Add-on anticholinergic therapy for residual nocturia in patients with lower urinary tract symptoms receiving α1-blocker treatment: a multi-centre, prospective, randomised study.

PURPOSE: To evaluate the efficacy and safety of imidafenacin (IM), a novel short half-life anticholinergic, as add-on therapy for male LUTS with nocturia and nocturnal polyuria. MATERIALS AND METHODS: This multicenter, prospective, randomized, open-labelled study was conducted and involved men who had frequency, urgency, and nocturia despite receiving a stable dose of α1-blocker for ≥1 month. Subjects were randomised to control (α1-blocker alone), IM twice/day (α1-blocker +0.1 mg imidafenacin twice daily), or IM nightly (α1-blocker plus 0.1 mg imidafenacin nightly) group; the treatment period was 8 weeks. Primary endpoints included improvements in night-time frequency and Nocturia Quality of Life Questionnaire (N-QOL) scores. Secondary endpoints included changes from the baseline in frequency volume chart variables, and post-void residual volume. RESULTS AND LIMITATIONS: Compared with the controls, IM twice/day and IM nightly patients had a significantly lower night-time frequency (changes from baseline: 0.1 ± 0.8 in control, -0.6 ± 0.9 in IM twice/day, and -0.4 ± 1.0 in IM nightly, p = 0.5227, 0.0006 and 0.0143, respectively). The hours of undisturbed sleep and N-QOL score were significantly improved in IM twice/day group, though not IM nightly group. Nocturnal urine volume was significantly reduced in IM nightly group, although total urine volume remained unchanged. CONCLUSIONS: A short half-life anticholinergic is suggested to be safe and effective as an add-on therapy for residual nocturia in patients with male LUTS receiving α1-blocker treatment. Anticholinergic administration nightly could reduce the nocturnal urine volume.

Botulinum toxin A injection for the treatment of neurogenic detrusor overactivity secondary to spinal cord injury: multi-institutional experience in Japan.

OBJECTIVES: To examine the efficacy and safety of onabotulinumtoxinA (Botox) injection into the bladder wall for the treatment of neurogenic detrusor overactivity secondary to spinal cord injury in Japanese patients. METHODS: We enrolled Japanese spinal cord injury patients with cystometrically confirmed neurogenic detrusor overactivity who experienced urinary incontinence at least once a week either because they were refractory to anticholinergics or had to discontinue treatment because of adverse events. Patients received 200 units of onabotulinumtoxinA injected into the bladder wall after a 2-week washout of anticholinergics, and urodynamic variables were assessed before and 1 month after injection. Catheterization and urinary incontinence data, as well as International Consultation on Incontinence Questionnaire-Short Form scores, were assessed before injection and every month thereafter until the cessation of treatment effects. RESULTS: The study enrolled 19 patients (13 men, six women, age range 22-67 years). One month after injection, the mean number of urinary incontinence episodes decreased from 4.3 to 1.5 times/day (P = 0.004), and the maximum cystometric capacity increased from 100 mL to 296 mL (P = 0.0004). The rate of effective cases whose daily urinary incontinence frequency was decreased to less than 50% was 74%. The duration of efficacy without anticholinergic medication ranged from 3 to 12 months (median 8.5 months). Clinically significant adverse events were not observed. CONCLUSIONS: The present findings show the efficacy and tolerability of onabotulinumtoxinA injection for the treatment of neurogenic detrusor overactivity in Japanese spinal cord injury patients.

Alpha 1-adrenoceptor blocker may improve not only voiding but also storage lower urinary tract symptoms caused by (125) I brachytherapy for prostate cancer.

Purpose. To assess changes in lower urinary tract symptoms (LUTS) within 1 year after brachytherapy in patients receiving alpha 1-adrenoceptor antagonists. Methods. We retrospectively evaluated 116 patients who underwent (125)I prostate brachytherapy in our institute. Seventy-one patients were treated with a combination of external beam radiation therapy and brachytherapy. Alpha 1-adrenoceptor antagonists were prescribed to all patients after brachytherapy. International Prostate Symptom Score (IPSS) forms and postvoid residual urine volume were recorded at all follow-up visits. Results. Forty-nine patients were given tamsulosin hydrochloride, 32 were given silodosin hydrochloride, and 35 were given naftopidil for up to 6 months after seed implantation. Patients given tamsulosin or naftopidil tended to show a higher peak IPSS and slower recovery to baseline values than those given silodosin. The patients given naftopidil showed an insufficient recovery in storage symptoms in naftopidil group in comparison with tamsulosin group at 3 months and with silodosin group at 6 and 9 months. Conclusions. In the management of LUT after brachytherapy, silodosin may provide a more favorable improvement. Silodosin and tamsulosin may have an advantage in improving not only voiding but also storage lower urinary tract symptoms after brachytherapy.

Diagnosis of complex renal cystic masses and solid renal lesions using PET imaging: comparison of 11C-acetate and 18F-FDG PET imaging.

PURPOSE: The study aims to assess the usefulness of PET with C-acetate and F-FDG to differentiate renal cell carcinoma (RCC) from complicated renal cysts. METHODS: Thirty-one patients were enrolled, 14 patients with complicated renal cysts (12 with Bosniak III and 2 with Bosniak IV) and 17 patients with 19 solid renal tumors. The patients underwent both C-acetate PET and FDG PET. Nephrectomy or partial nephrectomy was performed after the PET scans. RESULTS: In 29 patients, 32 renal lesions were diagnosed as RCC. Twenty-three of the 32 RCCs (72%) had positive C-acetate PET findings, whereas only 7 FDG PET studies were positive (22%). Considering the relationship between tumor size measured by macroscopic appearance of resected tumors and PET results, 22 of 25 (88%) tumors more than 1.5 cm showed positive C-acetate PET findings. In 12 patients with Bosniak III renal cysts, 10 renal lesions were diagnosed as RCC. In this subgroup, 5 of the 10 RCCs (50%) had positive C-acetate PET findings, whereas 2 RCCs (20%) had positive FDG PET findings. None of the cases with benign findings had positive C-acetate PET or FDG PET scans. CONCLUSIONS: C-acetate PET demonstrates a pronounced increase in tracer uptake in RCC, especially in renal tumors more than 1.5 cm, and displays a higher sensitivity than FDG PET. These preliminary data show that C-acetate may be a useful PET tracer to exclude RCC in complex renal cysts.

Factors influencing patient satisfaction with antimuscarinic treatment of overactive bladder syndrome: results of a real-life clinical study.

OBJECTIVES: To investigate patient satisfaction with antimuscarinic treatment of overactive bladder syndrome, and to identify factors having a significant influence on satisfaction. METHODS: A cross-sectional questionnaire survey was carried out to assess treatment satisfaction among male and female patients with overactive bladder (age ≥20 years) in the Hokuriku district of Japan. The overactive bladder symptom scores, treatment efficacies, adverse events (dry mouth and constipation), and patient satisfaction scores were investigated and compared among patients using different antimuscarinic therapeutics. RESULTS: In total, 977 survey respondents (52.6% men; mean age 73.6 years) received antimuscarinic treatment. The mean overactive bladder symptom score of these patients was 6.17; in addition, 32.3% patients were satisfied with their treatment, but 33.1% were dissatisfied. Factors having a significant influence on treatment satisfaction were sex (men were less satisfied), efficacy, adverse events and the overactive bladder symptom score. Constipation negatively influenced patient satisfaction to a greater extent than did dry mouth. Patient satisfaction varied according to the drug used. Constipation was less severe with the immediate-release-type agents (imidafenacin and oxybutynin) than with the extended-release-type (propiverine, solifenacin or tolterodine). CONCLUSIONS: Just one-third of Japanese Hokuriku patients with overactive bladder seem to be satisfied with their antimuscarinic treatment. Patient satisfaction is impaired by poor efficacy and the presence of adverse events; furthermore, constipation should be recognized as an adverse event that negatively influences patient satisfaction to a greater extent than dry mouth. Patient satisfaction differs according to the antimuscarinic agent used, with higher patient satisfaction being associated with less severe constipation.

[A case on hemodialysis with castration-resistant prostate cancer which responded to combination chemotherapy with docetaxel and prednisolone].

A 71-year-old man on hemodialysis was admitted for castration-resistant prostate cancer. He received chemotherapy with docetaxel(60mg/m2 every 3 weeks)and prednisolone(10mg/day). As severe adverse reactions due to chemotherapy were not encountered, he could receive chemotherapy in our outpatient clinic. A total of four courses of chemotherapy resulted in a 56% reduction in PSA, which was judged as PR. Chemotherapy with docetaxel and prednisolone can be safely carried out for a patient with castration-resistant prostate cancer, even while on hemodialysis with the usual dose of docetaxel.

[Successful treatment with docetaxel and prednisolone for paxlitaxel and carboplatin-resistant prostate cancer].

A 60-year-old man was examined at a local clinic for difficulty in urinating, and was diagnosed with prostatic hypertrophy. He was referred to our department because his prostate-specific antigen (PSA) level was elevated (276 ng/ml). His Gleason score was 4＋3, there was one bone metastasis in the left ileac bone, and multiple lung metastases were present. The patient was accordingly diagnosed with stage D2 prostate cancer. Lutenizing hormone-releasing hormone (LH-RH) analogue treatment was initiated in April 1999, and 9 months later the PSA level had decreased to 4.3 ng/ml. Six years and 9 months after the start of hormone therapy, the cancer had developed into castration-resistant prostate cancer and the PSA level had risen to 43.8 ng/ml. Paclitaxel-carboplatin therapy was therefore initiated. Eight months after the start of chemotherapy, the PSA level had decreased to 25.9 ng/ml, but 6 years and 1 month later it had risen to 925 ng/ml, and the chemotherapy was discontinued. Docetaxel-predonine therapy was initiated in March 2012. Three months after the start of chemotherapy, the PSA level had decreased to 3.1 ng/ml, and the bone metastasis was reduced.

Antidiuretic effect of antimuscarinic agents in rat model depends on C-fibre afferent nerves in the bladder.

UNLABELLED: WHAT'S KNOWN ON THE SUBJECT? AND WHAT DOES THE STUDY ADD?: Antichollnergic agents are anticipated to diminish storage symptoms, as well as nocturia. Nevertheless, the effect of this treatment on polyuria related to nocturia is not clear. By subgroup analysis of the data set from a phase III clinical trial of antimuscarinic agent for OAB patients in Japan, imidafenacin was found to improve nocturia with a reduction in nocturnal polyuria. This study adds the effects and underlying mechanism of antimuscarinic agents decreasing urine production through inhibition of C-fibre in the bladder of water-leaded rats. OBJECTIVE: To evaluate the effects and underlying mechanisms of antimuscarinic agents used to decrease in urine production in water-loaded rats. SUBJECTS AND METHODS: Urine production was measured using a cystostomy catheter in female Sprague-Dawley rats every 2 h. The effect of the antimuscarinic agents atropine, tolterodine and imidafenacin on urine production was investigated under water-loaded conditions, which were induced by i.p. injection of 15 mL saline. Blood samples were collected to determine the levels of antidiuretic hormone (ADH), aldosterone (ALD), atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) before, and 2 and 8 h after, antimuscarinic agent administration. To induce desensitization of C-fibre afferent nerves, resiniferatoxin (RTX)was injected s.c. or intravesically 2 days before experiments. RESULTS: Urine production increased and reached its maximum 2 h after 15 mL saline injection. Imidafenacin and tolterodine decreased urine production in water-loaded rats, but ADH, ALD, ANP and BNP levels were not different between imidafenacin-treated and vehicle-treated rats. The inhibitory effect on urine production was not found in RTX-treated rats. Atropine did not reduce urine production. CONCLUSION: These results suggest that antimuscarinic agents decrease urine volume through C-fibres in the bladder; thus, antimuscarinics with inhibitory effects on C-fibres could be beneficial for nocturia with nocturnal polyuria.

Surgical treatment of adrenal gland metastasis originating from small cell carcinoma of the urinary bladder.

We report a rare case of a solitary adrenal metastasis from small cell carcinoma of the urinary bladder that was successfully treated with surgical resection. A 71-year-old man was suffering from bladder tamponade for hematuria. Computed tomography (CT) revealed a bladder tumor at the left wall. The patients underwent radical cystectomy. Histopathological results were obtained in small cell carcinoma of the bladder with muscle invasion. Thus, he received two courses of adjuvant etoposide and cisplatin chemotherapy, followed by the regimen for small cell lung cancer. Seven months after surgery, follow-up CT showed a gradually enlarged mass enhanced heterogeneously in the right adrenal gland. There was a solitary adrenal metastasis without any other metastasis; therefore, we performed right laparoscopic adrenalectomy. The patient has remained uneventful for four years after the adrenal gland surgery. For patients who have a solitary adrenal metastasis, adrenalectomy may provide a survival benefit.

IPSS is lower in hypertensive patients treated with angiotensin-II receptor blocker: posthoc analyses of a lower urinary tract symptoms population.

AIMS: The existence of Angiotensin-II (Ang-II) receptors in the bladder wall and the pronounced contractile effect of Ang-II on the human detrusor muscle have been well established. Studies have presented the role of Ang-II as a mediator in smooth muscle growth and collagen production in the bladder with outlet obstruction. We investigated the associations between male lower urinary tract symptoms (LUTS) and hypertension (HT), and examined whether the medications used for HT treatment, particularly Ang-II receptor blockers (ARBs) influence LUTS. METHODS: Among 4,298 men with LUTS who were nominated to participate in a Japanese study using the International Prostate Symptom Score (IPSS) to gain information on the effects and the safety of silodosin, a total of 3,790 men for whom a baseline IPSS was available were sub-analyzed. We analyzed the influence of HT treatment on IPSSs. RESULTS: HT was the most common comorbidity (1,122 men, 29.6%), and 769 men (20.3%) were receiving some kinds of medication for the treatment. We found that the IPSS was lower in patients being treated for HT with ARB than in hypertensive patients who were not receiving any medication (16.8 ± 6.8 vs. 18.3 ± 6.6, P < 0.01). The baseline I-PSS in patients treated for HT with angiotensin converting enzyme inhibitor (ACE-I), calcium channel blocker (CCB), and normotensive patients were 18.3, 19.6, and 18.1, respectively. CONCLUSION: The IPSS is lower in patients with HT treated with ARB. Other drugs for HT, including ACE-I and CCB, did not improve the IPSS.

Spontaneous Contractile Activity of the Detrusor Muscle and Its Role in the Pathogenesis of Overactive Bladder Syndrome.

There is accumulated evidence that spontaneous contractions (SCs) in the bladder wall are associated with afferent nerve firing in the bladder. The role of the urothelium in bladder sensation might be restricted to pathological conditions, such as interstitial cystitis or chemical cystitis in which the release of urothelium-derived mediators such as adenosine triphosphate is increased. Recent publications imply that SCs in bladders with detrusor overactivity due to spinal cord injury or bladder outlet obstruction are modulated by intracellular signal transduction mechanisms such as the RhoA/Rho-kinase pathway, denervation-supersensitivity to acetylcholine, changes in ion channel activity, enhanced gap-junctional intercellular communication, alterations in interstitial cells of Cajal, the actions of local mediators in the detrusor and the influence of the urothelium. Spontaneous contractions and possible consequent afferent nerve firing might participate in the generation of overactive bladder syndrome.