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Bladder Activity (bladder + activity)
Selected AbstractsTMAOase Activity of European Hake (Merluccius merluccius) Organs: Influence of Biological Condition and SeasonJOURNAL OF FOOD SCIENCE, Issue 9 2002M. Rey-Mansilla ABSTRACT: Trimethylamine N-oxide demethylase (TMAOase) activity of several internal organs of hake were studied for 2 consecutive y. The correlation between enzymatic activity and season of year, sex, weight, and length were analyzed. While kidney and spleen showed the highest activities, liver, heart, bile, and gall bladder activities were much lower, and in some cases they were below the detection limit. A correlation between TMAOase activity of kidney and season was found. During winter and spring (February to May), the months matching the spawning peak, high activities were detected, while in summer months the activity level was lower. TMAOase activity in the rest of the organs did not seem to have a seasonal influence. Keywords: TMAOase, season, biological condition, hake, soluble protein [source] Changes of bladder activity and glycine levels in the lumbosacral cord after partial bladder outlet obstruction in ratsINTERNATIONAL JOURNAL OF UROLOGY, Issue 9 2008Minoru Miyazato Objectives: We investigated the time course of changes in bladder activity as well as in spinal and serum levels of glutamate and glycine after partial bladder outlet obstruction (BOO) in rats. Methods: A total of 36 female rats were divided into six groups: sham operation (control); 3 days, 14 days, and 28 days after BOO; 3 days and 28 days after relief of BOO. Under urethane anesthesia, isovolumetric cystometry was carried out in each group. Then, spinal and serum levels of glutamate and glycine were measured. Results: The interval between bladder contractions was shorter in all of the groups compared with the control group. The amplitude and duration of bladder contractions was decreased at 3 days, 14 days, and 28 days after BOO, and at 3 days after relief of BOO. Spinal and serum glutamate levels showed no changes. However, the spinal glycine level was decreased at 14 days and 28 days after BOO, and at 28 days after relief of BOO. Serum glycine level was also decreased at 28 days after BOO and 28 days after relief of BOO. Conclusions: Detrusor overactivity during the chronic phase of partial BOO is partly caused by a decrease of glycinergic neuronal activity in the lumbosacral cord. A 3-day period of BOO produces detrusor overactivity, which might be due to an irreversible decrease of spinal glycinergic neuronal activity. [source] Intrathecal glutamate promotes glycinergic neuronal activity and inhibits the micturition reflex in urethane-anesthetized ratsINTERNATIONAL JOURNAL OF UROLOGY, Issue 12 2006KATSUHIRO ASHITOMI Objectives: In order to clarify the role of glutamate in the micturition reflex and in glutamatergic and glycinergic neuronal activity, we examined the effects of intrathecal (IT) injection of glutamate or MK-801 (an N- methyl-D-aspartate receptor antagonist) on bladder activity and on the glutamate and glycine levels in the lumbosacral cord of female rats with or without acute lower thoracic spinal cord injury (SCI). Methods: Under urethane anesthesia, isovolumetric cystometry was performed in rats with or without SCI before and after IT injection of glutamate or MK-801 at the lumbosacral cord level. The glutamate and glycine levels of the whole lumbosacral cord were measured after IT injection of glutamate or MK-801 in both groups. Results: In intact rats, IT glutamate (100 µg) prolonged the interval between bladder contractions and decreased the amplitude of contractions. IT MK-801 (3,100 µg) also prolonged the interval between bladder contractions and decreased the amplitude in intact rats. In SCI rats, cystometry demonstrated the disappearance of bladder contractions, and the glycine level in the lumbosacral cord was elevated. In intact rats, IT glutamate (0.3,100 µg) increased the glycine level in the lumbosacral cord. On the other hand, IT MK-801 (3,100 µg) decreased both glutamate and glycine levels in intact and SCI rats. Conclusions: These results suggest that glutamatergic neurons have stimulatory projections to both glutamatergic and glycinergic neurons in the lumbosacral cord, and that glutamatergic neurons inhibit the micturition reflex by stimulating glycinergic neurons. [source] Urodynamic evaluation of fesoterodine metabolite, doxazosin and their combination in a rat model of partial urethral obstructionBJU INTERNATIONAL, Issue 2 2010Claudius Füllhase OBJECTIVE To evaluate the urodynamic effects of fesoterodine, a new antimuscarinic agent, alone and combined with doxazosin, in a rat model of partial urethral obstruction (PUO), as 35,83% of men with bladder outlet obstruction (BOO) secondary to benign prostatic hyperplasia (BPH) have overactive bladder (OAB) syndrome, and as the combination of ,1 -adrenoceptor- and muscarinic-receptor antagonists has been proposed to be beneficial for these patients. MATERIALS AND METHODS Thirty-seven male Sprague-Dawley rats (250 g) had surgically induced PUO; 2 weeks later they were evaluated by cystometry with no anaesthesia or any restraint. After a 1-h period either 5-hydroxymethyl tolterodine (5-HMT, the active metabolite of fesoterodine, previously known as SPM 7605), doxazosin or a combination of both, was given intravenously (0.1 mg/kg body weight), and cystometry was continued for another 45 min. Fifteen healthy, age-matched rats served as a control. RESULTS At 2 weeks after surgery the obstructed rats had an greater bladder weight, threshold pressure (TP) and micturition frequency (MF), and lower bladder capacity (BCap) and micturition volume (MV) than the controls. 5-HMT did not cause urinary retention in obstructed rats, but decreased TP, maximum pressure (MP), spontaneous bladder activity (SA) and, paradoxically, increased MF. Doxazosin alone decreased TP, MP, MF and increased BCap and MV. 5-HMT and doxazosin together did not depress the ability to empty the bladder, and showed decreased TP, MP and SA. CONCLUSIONS 5-HMT, alone and in combination, did not impair the voiding ability in obstructed rats. Doxazosin counteracted some of the ,negative' effects of 5-HMT in this model (increase of MF) and did not attenuate the ,positive' effects (decrease of bladder SA). In this model, the combination of 5-HMT and doxazosin appeared to be urodynamically safe and well tolerated. [source] Type 4 phosphodiesterase inhibitor suppresses experimental bladder inflammationBJU INTERNATIONAL, Issue 10 2008Takeya Kitta OBJECTIVE To evaluate the effects of orally administered YM976, a specific inhibitor of type 4 phosphodiesterase (PDE4), on bladder activity in a rat model with hydrochloric acid (HCl)-induced cystitis (IC), hypothesizing that a PDE4 inhibitor might suppress bladder overactivity and bladder pain responses in bladder-hypersensitive disorders such as IC. MATERIALS AND METHODS Wistar rats with HCl-induced IC were treated with YM976 or vehicle and their voiding observed and assessed by cystometry. The severity of bladder inflammation (BI) was quantified using the BI index (BII), which comprises three factors (oedema, leukocyte infiltration and haemorrhage). Nociceptive neural activity was also examined using an immunohistochemical study of spinal c-fos expression. RESULTS YM976 significantly reduced the number of voids, and the volume per void was significantly higher than in control (vehicle) group. Cystometry showed a significant increase in bladder capacity, voided volume and voiding efficiency, and a decrease in the amplitude of voiding pressure in rats treated with YM976. All BII scores were significantly lower in the YM976 than in the control group. c-fos expression in the spine was less in the YM976 than in the control group. CONCLUSIONS Oral administration of YM976 significantly improved the voiding behaviour and histological damage in rats with IC induced by HCl. These results indicate that PDE4 inhibitor might be effective in relieving bladder symptoms with IC. [source] Phosphodiesterase-linked inhibition of nonmicturition activity in the isolated bladderBJU INTERNATIONAL, Issue 9 2004J.I. Gillespie Over the past few months Gillespie has published several papers in the BJU International investigating the overactive bladder and BOO, using novel models and theories. This next paper continues these concepts and shows that the mechanisms influencing the frequency of agonist-induced phasic activity in the isolated bladder model is slowed by cAMP. These findings will have important implications in future pharmacological strategies in the overactive bladder. OBJECTIVE To explore the influence of intracellular cAMP on phasic activity in the isolated bladder (phasic rises in intravesical pressure associated with waves of contraction and local stretches that can be activated by muscarinic or nicotinic agonists), as it has been argued that this activity underlies nonmicturition contractions, and that it contributes to the generation and modulation of afferent nerve activity. MATERIALS AND METHODS Isolated whole bladders from female guinea pigs (270,300 g) were cannulated via the urethra and suspended in a chamber containing oxygenated Tyrode solution at 33,35 °C. Bladder pressure was recorded and pharmacological agents added to the solution bathing the abluminal surface of the bladder. RESULTS Forskolin (1,3 µmol/L), an activator of adenyl cyclase, reduced the frequency and amplitude of the phasic activity induced by the muscarinic agonist arecaidine (300 nmol/L). There were similar changes in frequency and amplitude in bladders exposed to the nonspecific phosphodiesterase (PDE) inhibitor iso-butyl-methyl-xanthene (IBMX). The actions of specific PDE inhibitors were explored to assess which isoenzymes might be responsible for regulating phasic activity. ENHA (PDE-2), zaprinast (PDE-5, -6, -8, -9 and -11) and siguazodan (PDE-3) had no effect. Zardavarine (PDE-3, -4) and Ro 20-1724 (PDE-4) reduced both the frequency and amplitude of the phasic activity. Nerve-mediated rises in intravesical pressure were also inhibited by Ro 20-1724, and the inhibition was more pronounced at 6.5 Hz than at 30 Hz stimulation. Ro 20-1724 inhibited nerve-mediated fluctuations induced by prolonged (200 s) stimulation at 6.5 Hz. CONCLUSION The mechanisms influencing the frequency of agonist-induced phasic activity in the isolated bladder are slowed by cAMP. Degradation of intracellular cAMP in the cells responsible for phasic activity appears to involve primarily PDE-4. The importance of these observations in relation to the overall physiological regulation of the bladder are discussed, and the possible importance of these findings in the development of pharmacological strategies to modulated bladder activity reviewed. [source] Dual modulation of urinary bladder activity and urine flow by prostanoid EP3 receptors in the conscious ratBRITISH JOURNAL OF PHARMACOLOGY, Issue 1 2009MJ Jugus Background and purpose:, Cyclooxygenase inhibitors function to reduce levels of prostaglandin E2 (PGE2) and are broadly efficacious in models of bladder overactivity. We therefore investigated a regulation of urinary bladder function in conscious rats by modulation of the EP3 receptor for PGE2. Experimental approach:, The activity of the EP3 receptor agonist GR63799X, and EP3 receptor antagonists, CM9 and DG041, at recombinant EP3 receptors was evaluated in vitro. In vivo, intraduodenal dosing during conscious, continuous-filling cystometry of spontaneously hypertensive rats was utilized to determine the urodynamic effect of EP3 receptor modulation. Key results:, GR63799X dose-dependently (0.001,1 mg·kg,1) reduced bladder capacity, as indicated by a reduction in both the micturition interval and volume of urine per void. In contrast, CM9 (10 and 30 mg·kg,1) and DG041 (30 mg·kg,1) enhanced bladder capacity, as indicated by significantly longer micturition intervals and larger void volumes. CM9 and DG041 inhibited the responses to GR63799X supporting the in vivo activity of these pharmacological agents at the EP3 receptor. In addition to its effect on bladder capacity, GR63799X increased endogenous urine production. Intra-arterial infusion of saline mimicked the enhancement of urine flow observed with GR63799X, and the response was inhibited by CM9. Conclusions and implications:, These data support the EP3 receptor as a modulator of urinary bladder activity in the conscious rat, and in addition, indicate a role for EP3 receptor activity in regulating urine flow. [source] | ||||||||||