THE ROLE OF INTERLEUKIN-6 ON THE CONTRACTILE RESPONSES OF RAT URINARY BLADDER

2006 ◽  
Vol 5 (2) ◽  
pp. 79
Author(s):  
S.C. Myung ◽  
M.Y. Lee ◽  
M.K. Lee ◽  
S.H. Ahn ◽  
T.H. Kim ◽  
...  
Keyword(s):  
Urinary Bladder ◽  
Interleukin 6 ◽  
Rat Urinary Bladder ◽  
Contractile Responses

scholarly journals Expression and functional role of Rho-kinase in rat urinary bladder smooth muscle

2003 ◽  
Vol 138 (5) ◽  
pp. 757-766 ◽  
Author(s):  
Alexandra Wibberley ◽  
Zunxuan Chen ◽  
Erding Hu ◽  
J Paul Hieble ◽  
Timothy D Westfall
Keyword(s):  
Smooth Muscle ◽  
Urinary Bladder ◽  
Functional Role ◽  
Rho Kinase ◽  
Bladder Smooth Muscle ◽  
Rat Urinary Bladder ◽  
Urinary Bladder Smooth Muscle

Excitation of rat urinary bladder by coaxial electrodes and by chemical agents

1963 ◽  
Vol 204 (4) ◽  
pp. 727-731 ◽  
Author(s):  
F. G. Carpenter
Keyword(s):  
Urinary Bladder ◽  
Motor Nerve ◽  
Water Pressure ◽  
Rat Urinary Bladder ◽  
Contractile Responses ◽  
Ringer’S Solution ◽  
Chemical Agents ◽  
Site Of Action ◽  
Electrical Pulses ◽  
Electrical Stimuli

Electrical stimulation of an isolated rat urinary bladder in tris buffered Ringer's solution by coaxial electrodes elicits contractile responses amounting to 70–130 cm of water pressure. If the Ringer's solution is replaced by isotonic K2SO4 solution, pressures of 60–110 cm water pressure are developed. Responses elicited by low stimulating frequencies (.5–2.5/sec) and by K2SO4 are potentiated by physostigmine, however, 2 mg/liter atropine throughout the entire frequency range of .5–10/sec is without effect. The stimulating actions of K2SO4 and electrical stimuli are dependent upon the availability of Ca++. Responses to electric stimuli are believed to be mediated by way of cholinergic neural elements, those from K+ by a depolarization of the muscle fibers. To a more limited extent the contractile responses resulting from acetylcholine (ACh) are dependent upon Ca++ and contractures are also produced by ACh in bladders suspended in isotonic K2SO4. Conversely, electrical pulses or K2SO4 are effective stimuli in the presence of quantities of ACh or carbamylcholine sufficient to produce maximal responses. This suggests a different site of action for exogenous ACh as opposed to endogenous mediator released from cholinergic motor nerve terminals during motor nerve stimulation.

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.

Urothelial acetylcholine involvement in ATP-induced contractile responses of the rat urinary bladder

2017 ◽  
Vol 809 ◽  
pp. 253-260 ◽  
Author(s):  
Johanna Stenqvist ◽  
Michael Winder ◽  
Thomas Carlsson ◽  
Patrik Aronsson ◽  
Gunnar Tobin
Keyword(s):  
Urinary Bladder ◽  
Rat Urinary Bladder ◽  
Contractile Responses

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

The role of cholinesterases in rat urinary bladder contractility

2003 ◽  
Vol 31 (3) ◽  
pp. 223-226 ◽  
Author(s):  
Tsutomu Nakahara ◽  
Yuko Kubota ◽  
Kenji Sakamoto ◽  
Kunio Ishii
Keyword(s):  
Urinary Bladder ◽  
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.

scholarly journals Stimulation of β3-adrenoceptors relaxes rat urinary bladder smooth muscle via activation of the large-conductance Ca2+-activated K+ channels

2008 ◽  
Vol 295 (5) ◽  
pp. C1344-C1353 ◽  
Author(s):  
Kiril L. Hristov ◽  
Xiangli Cui ◽  
Sean M. Brown ◽  
Lei Liu ◽  
Whitney F. Kellett ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Urinary Bladder ◽  
Bk Channels ◽  
Bk Channel ◽  
Bladder Smooth Muscle ◽  
Rat Urinary Bladder ◽  
Urinary Bladder Smooth Muscle ◽  
Brl 37344 ◽  
Stimulation Of

We investigated the role of large-conductance Ca2+-activated K+ (BK) channels in β3-adrenoceptor (β3-AR)-induced relaxation in rat urinary bladder smooth muscle (UBSM). BRL 37344, a specific β3-AR agonist, inhibits spontaneous contractions of isolated UBSM strips. SR59230A, a specific β3-AR antagonist, and H89, a PKA inhibitor, reduced the inhibitory effect of BRL 37344. Iberiotoxin, a specific BK channel inhibitor, shifts the BRL 37344 concentration response curves for contraction amplitude, net muscle force, and tone to the right. Freshly dispersed UBSM cells and the perforated mode of the patch-clamp technique were used to determine further the role of β3-AR stimulation by BRL 37344 on BK channel activity. BRL 37344 increased spontaneous, transient, outward BK current (STOC) frequency by 46.0 ± 20.1%. In whole cell mode at a holding potential of Vh = 0 mV, the single BK channel amplitude was 5.17 ± 0.28 pA, whereas in the presence of BRL 37344, it was 5.55 ± 0.41 pA. The BK channel open probability was also unchanged. In the presence of ryanodine and nifedipine, the current-voltage relationship in response to depolarization steps in the presence and absence of BRL 37344 was identical. In current-clamp mode, BRL 37344 caused membrane potential hyperpolarization from −26.1 ± 2.1 mV (control) to −29.0 ± 2.2 mV. The BRL 37344-induced hyperpolarization was eliminated by application of iberiotoxin, tetraethylammonium or ryanodine. The data indicate that stimulation of β3-AR relaxes rat UBSM by increasing the BK channel STOC frequency, which causes membrane hyperpolarization and thus relaxation.

Sign in / Sign up

Export Citation Format

Share Document