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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 12 weeks. 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 E 2 (PGE 2 ) 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 PGE 2 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 PGE 2 release from the urothelium via suppression of BBF.

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.

INTRODUCTION AND OBJECTIVES: Insulin-like growth factor-1 (IGF-1) plays an important role in cell proliferation, survival and regeneration in various tissues. We recently reported that IGF-1 treatment accelerates recovery from stress urinary incontinence (SUI) induced by stimulated child birth trauma in rats. Because IGF1 reportedly interacts with estrogen, in the present study, we examined whether ovariectomy (OVX) affected the therapeutic effect of IGF-1 on the recovery of SUI induced by simulated childbirth injury in rats. METHODS: Female Sprague-Dawley rats (8 weeks) underwent bilateral OVX or sham operation. After 2 weeks, simulated birth trauma was induced by vaginal distension (VD). Human recombinant IGF-1 (hrIGF-1) (150mg/kg/day) was continuously delivered from 1 day before VD for 7 days using subcutaneous osmotic pumps. At 7 and 14 days after VD, urethral responses were measured using a microtransducer-tipped catheter inserted to the middle urethra from the urethral orifice. The amplitude of urethral responses during sneezing (A-URS), urethral baseline pressure (UBP) and leak point pressure at the time of sneeze (S-LPP) were evaluated. Sneeze was induced by a rat whisker inserted into the nostril. RESULTS: At 7 days after VD, A-URS and UBP, which were reduced by VD, were significantly increased in the sham+IGF-1 group compared to the OVX+vehicle group (A-URS: 14.7 vs. 7.4 cmH2O, UBP: 20.2 vs. 12.7 cmH2O); however there were no significant difference in A-URS or UBP between OVX+IGF-1 and OVX+vehicle groups (Figure). Moreover, S-LPP in the sham+IGF-1 group was significantly elevated compared to the OVX+vehicle group (63.9 vs. 50.9cmH2O) although sneeze-induced SUI was still observed in all groups. At 14 days after VD, sneeze-induced SUI was observed in OVX+vehicle (40%) and OVX+IGF-1 groups (50%) whereas SUI was not observed in sham+vehicle and sham+IGF-1 groups (0%) (Figure). CONCLUSIONS: The therapeutic effects of IGF-1 on SUI induced by simulated childbirth injury were reduced when estrogen deficiency was induced by OVX in rats, suggesting that the efficacy of IGF-1 treatment for childbirth-related SUI could be strengthened in the presence of estrogen.

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.To evaluate the effects and underlying mechanisms of antimuscarinic agents used to decrease in urine production in water-loaded rats.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.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.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.

Primary amyloidosis of the seminal vesicle is a rare disease entity. We report here a case of localized seminal vesicle amyloidosis with hematospermia. A 66-year-old man visited our hospital with a chief complaint of hematospermia. T2 weighted magnetic resonance imaging (MRI) showed a hypointensity mass in the left seminal vesicle. Needle biopsy revealed amyloidosis of the seminal vesicle. Without any specific treatment, the mass lesion disappeared on MRI, and hematospermia was improved.