Role of Nitric Oxide in Urinary Bladder Function: Effect of L-Arginine

2007 ◽  
Vol 78 (1) ◽  
pp. 30-36 ◽  
Author(s):  
Catherine Whitbeck ◽  
Paul Chichester ◽  
Rebekah Sokol ◽  
Robert M. Levin
Keyword(s):  
Nitric Oxide ◽  
Urinary Bladder ◽  
Bladder Function

1450: Role of Nitric Oxide in the Urinary Bladder Function: Effect of Argenine

2006 ◽  
Vol 175 (4S) ◽  
pp. 468-468
Author(s):  
Catherine Whitbeck ◽  
Paul Chichester ◽  
Rebekah Sokol ◽  
Robert M. Levin
Keyword(s):  
Nitric Oxide ◽  
Urinary Bladder ◽  
Bladder Function

scholarly journals Uropathogenic Escherichia coli-Induced Inflammation Alters Mouse Urinary Bladder Contraction via an Interleukin-6-Activated Inducible Nitric Oxide Synthase-Related Pathway

2009 ◽  
Vol 77 (8) ◽  
pp. 3312-3319 ◽  
Author(s):  
Te I. Weng ◽  
Hsiao Yi Wu ◽  
Pei Ying Lin ◽  
Shing Hwa Liu
Keyword(s):  
Nitric Oxide ◽  
Escherichia Coli ◽  
Urinary Tract Infection ◽  
Urinary Tract ◽  
Urinary Bladder ◽  
Tract Infection ◽  
Interleukin 6 ◽  
Electrical Field Stimulation ◽  
E Coli

ABSTRACT Escherichia coli is the most common cause of urinary tract infection. Elevated blood and urine interleukin-6 (IL-6) levels have been shown in inflammatory urinary tract diseases. The role of IL-6 in mediating the urodynamic dysfunction in response to E. coli-induced urinary tract infection has not yet been fully elucidated. In this study, we investigated the role of IL-6 in the nitric oxide (NO)-triggered alteration of contractile responses in the urinary bladder under an E. coli-induced inflammatory condition. The electrical field stimulation (EFS)-evoked contractions of the isolated detrusor strips, and immunoblotting for detecting protein expression in the bladders was measured short term (1 h) or long term (6 or 24 h) after intraperitoneal injection of E. coli endotoxin (lipopolysaccharide [LPS]) or intravesical instillation of human pyelonephritogenic E. coli-J96 (O4:K6) strain or LPS into mice. IL-6 and NO productions were increased in the urinary bladders of mice 1 to 24 h after LPS or E. coli-J96 treatment. Inducible NO synthase (iNOS) expression and protein kinase C (PKC) activation and EFS-evoked detrusor contractions were increased in the bladders at 6 h after LPS or E. coli-J96 treatment, which could be reversed by anti-IL-6 antibody and iNOS inhibitor aminoguanidine. At 1 h after LPS administration, bladder NO generation, endothelial NOS expression, and EFS-evoked detrusor contractions were effectively increased, whereas anti-IL-6 antibody could not reverse these LPS-induced responses. These results indicate that IL-6 may play an important role in the iNOS/NO-triggered PKC-activated contractile response in urinary bladder during E. coli or LPS-induced inflammation.

scholarly journals A possible role of the cholinergic and purinergic receptor interaction in the regulation of the rat urinary bladder function

2012 ◽  
Vol 32 (6) ◽  
pp. 421-431 ◽  
Author(s):  
Ágnes Jenes ◽  
Ferenc Ruzsnavszky ◽  
Andrea Telek ◽  
Gyula P. Szigeti ◽  
László Csernoch
Keyword(s):  
Urinary Bladder ◽  
Purinergic Receptor ◽  
Bladder Function ◽  
Receptor Interaction ◽  
Rat Urinary Bladder

scholarly journals Role of p75NTR in female rat urinary bladder with cyclophosphamide-induced cystitis

2008 ◽  
Vol 295 (6) ◽  
pp. F1778-F1789 ◽  
Author(s):  
Mary Beth Klinger ◽  
Margaret A. Vizzard
Keyword(s):  
Urinary Bladder ◽  
Intravesical Instillation ◽  
Bladder Function ◽  
Neurotrophin Receptor ◽  
P75 Neurotrophin Receptor ◽  
Female Rat ◽  
Rat Urinary Bladder ◽  
Micturition Reflex ◽  
Reflex Pathways

Previous studies demonstrated changes in urinary bladder neurotrophin content and upregulation of neurotrophin receptors, TrkA and the p75 neurotrophin receptor (p75NTR), in micturition reflex pathways after cyclophosphamide (CYP)-induced cystitis. p75NTR can bind nerve growth factor (NGF) and modulate NGF-TrkA binding and signaling. We examined p75NTR expression and the role of p75NTR in the micturition reflex in control and CYP-treated rats. p75NTR Immunoreactivity was present throughout the urinary bladder. CYP-induced cystitis (4 h, 48 h, chronic) increased ( P ≤ 0.05) p75NTR expression in whole urinary bladder as shown by Western blotting. The role of p75NTR in bladder function in control and CYP-treated rats was determined using conscious cystometry and immunoneutralization or PD90780, a compound known to specifically block NGF binding to p75NTR. An anti-p75NTR monoclonal antibody or PD90780 was infused intravesically and cystometric parameters were evaluated. Both methods of p75NTR blockade significantly ( P ≤ 0.05) decreased the intercontraction interval and void volume in control and CYP-treated rats. Intravesical infusion of PD90780 also significantly ( P ≤ 0.001) increased intravesical pressure and increased the number of nonvoiding contractions during the filling phase. Control intravesical infusions of isotype-matched IgG and vehicle were without effect. Intravesical instillation of PD90780 significantly ( P ≤ 0.01) reduced the volume threshold to elicit a micturition contraction in control rats (no inflammation) and CYP-treated in a closed urinary bladder system. These studies demonstrate 1) ubiquitous p75NTR expression in urinary bladder and increased expression with CYP-induced cystitis and 2) p75NTR blockade at the level of the urinary bladder produces bladder hyperreflexia in control and CYP-treated rats. The overall activity of the urinary bladder reflects the balance of NGF-p75NTR and NGF-TrkA signaling.

Effect of ischemia-reperfusion on contractile function of rat urinary bladder: Possible role of nitric oxide

Life Sciences ◽  
1998 ◽  
Vol 62 (11) ◽  
pp. PL149-PL156 ◽  
Author(s):  
Motoaki Saito ◽  
Kouichirou Wada ◽  
Yoshinori Kamisaki ◽  
Ikuo Miyagawa
Keyword(s):  
Nitric Oxide ◽  
Urinary Bladder ◽  
Contractile Function ◽  
Ischemia Reperfusion ◽  
Rat Urinary Bladder

scholarly journals Coupled Nitric Oxide and Autonomic Receptor Functional Responses in the Normal and Inflamed Urinary Bladder of the Rat

2012 ◽  
pp. 371-380 ◽  
Author(s):  
R. VESELÁ ◽  
H. ASKLUND ◽  
P. ARONSSON ◽  
M. JOHNSSON ◽  
V. WSOL ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Urinary Bladder ◽  
The Body ◽  
Bladder Function ◽  
Detrusor Muscle ◽  
Functional Responses ◽  
Nitric Oxide Synthase Inhibitor ◽  
Parasympathetic Nerve ◽  
Contractile Responses

Both divisions of the autonomic nervous system are involved in regulation of urinary bladder function. Several substances, other than noradrenaline and acetylcholine, seem to play important roles in physiology and pathophysiology of lower urinary tract. In the current study, we aimed to examine if there exist interplays between nitric oxide (NO) and autonomic transmitters and if such interactions vary in different parts of the urinary bladder in healthy and cyclophosphamide (CYP)-induced cystitic rats; when administered to the animals (100 mg/kg; i.p.), the cytotoxic CYP metabolite acrolein induces bladder inflammation. In the current study a series of in vitro functional studies were performed on detrusor muscle strip preparations. Stimulation with electrical field stimulation (EFS), methacholine, adenosine 5´-triphosphate (ATP), and adrenaline evoked contractile responses in isolated bladder preparations that were significantly reduced in cyclophosphamide (CYP)-treated rats. While the nitric oxide synthase inhibitor Nω nitro-L-arginine (L-NNA; 10-4 M) did not affect contractile responses in normal, healthy strip preparations, it significantly increased the contractile responses to EFS, methacholine and adrenaline, but not to ATP, in the bladders from the CYP-treated rats. In the CYP-treated rats, the ATP-evoked relaxatory part of its dual response (an initial contraction followed by a relaxation) was 6-fold increased in comparison with that of normal preparations, whereas the isoprenaline relaxation was halved in the CYP-treated. While L-NNA (10-4 M) had no effect on the isoprenaline-evoked relaxations, it reduced the ATP-evoked relaxations in strip preparations from the bladder body of CYP-treated rats. Stimulation of β2- and β3 adrenoceptors evoked relaxations and both responses were reduced in cystitis, the latter to a larger extent. In the trigone, the reduced ATP-evoked contractile response in the inflamed strips was increased by L-NNA, while L NNA had no effect on the ATP-evoked relaxations, neither on the relaxations in healthy nor on the larger relaxations in the inflamed trigone. The study shows that both contractile and relaxatory functions are altered in the state of inflammation. The parasympathetic nerve-mediated contractions of the body of the bladder, evoked by the release of ATP and acetylcholine, were substantially reduced in cystitis. The relaxations to β-adrenoceptor and purinoceptor stimulation were also reduced but only the ATP-evoked relaxation involved NO.

scholarly journals Overexpression of NGF in mouse urothelium leads to neuronal hyperinnervation, pelvic sensitivity, and changes in urinary bladder function

2010 ◽  
Vol 298 (3) ◽  
pp. R534-R547 ◽  
Author(s):  
Birthe Schnegelsberg ◽  
Tung-Tien Sun ◽  
Gary Cain ◽  
Anindya Bhattacharya ◽  
Philip A. Nunn ◽  
...  
Keyword(s):  
Mast Cells ◽  
Urinary Bladder ◽  
Transgenic Mice ◽  
Bladder Dysfunction ◽  
Sympathetic Neurons ◽  
Nerve Fibers ◽  
Bladder Function ◽  
Sensory Afferents ◽  
Urinary Bladder Dysfunction

NGF has been suggested to play a role in urinary bladder dysfunction by mediating inflammation, as well as morphological and functional changes, in sensory and sympathetic neurons innervating the urinary bladder. To further explore the role of NGF in bladder sensory function, we generated a transgenic mouse model of chronic NGF overexpression in the bladder using the urothelium-specific uroplakin II (UPII) promoter. NGF mRNA and protein were expressed at higher levels in the bladders of NGF-overexpressing (NGF-OE) transgenic mice compared with wild-type littermate controls from postnatal day 7 through 12–16 wk of age. Overexpression of NGF led to urinary bladder enlargement characterized by marked nerve fiber hyperplasia in the submucosa and detrusor smooth muscle and elevated numbers of tissue mast cells. There was a marked increase in the density of CGRP- and substance P-positive C-fiber sensory afferents, neurofilament 200-positive myelinated sensory afferents, and tyrosine hydroxylase-positive sympathetic nerve fibers in the suburothelial nerve plexus. CGRP-positive ganglia were also present in the urinary bladders of transgenic mice. Transgenic mice had reduced urinary bladder capacity and an increase in the number and amplitude of nonvoiding bladder contractions under baseline conditions in conscious open-voiding cystometry. These changes in urinary bladder function were further associated with an increased referred somatic pelvic hypersensitivity. Thus, chronic urothelial NGF overexpression in transgenic mice leads to neuronal proliferation, focal increases in urinary bladder mast cells, increased urinary bladder reflex activity, and pelvic hypersensitivity. NGF-overexpressing mice may, therefore, provide a useful transgenic model for exploring the role of NGF in urinary bladder dysfunction.

C34 Role of TRPV3 in urinary bladder function and sensory signaling

2013 ◽  
Vol 12 (4) ◽  
pp. e1142, C34
Author(s):  
M.K. Lam ◽  
T.K. Mann-Gow ◽  
K. Zvarová ◽  
X. Zhen ◽  
M.M. Moran ◽  
...  
Keyword(s):  
Urinary Bladder ◽  
Bladder Function ◽  
Sensory Signaling
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