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1 remodeling of urinary bladder smooth muscle (detrusor).
2 uscles, and phasic contractions occur in the detrusor.
3 tic hyperplasia (BPH), an overactive bladder detrusor (a syndrome of urinary urgency and frequency),
4 iding onset, peak pressure, and elevation in detrusor-activated bladder pressure from the end of blad
5 ion, capacity, compliance, and inappropriate detrusor activity during filling; (3) urethral pressure
6 isplayed increases in bladder compliance and detrusor activity, upregulations of IL-2, Trpa1 and Itga
7 replicated the improved coordination between detrusor and external urethral sphincter activity that h
8 tion consists of an inhibitory effect on the detrusor and presumably the lower rectum resulting from
9 l voiding with an uncoordination between the detrusor and urinary sphincter, and enuresis.
10 ssion in nerve fibers in the urinary bladder detrusor and urothelium was decreased or eliminated afte
11  activation of smooth muscle of the bladder (detrusor) and striated muscle of the external urethral s
12 tween layers of the bladder wall (mucosa vs. detrusor) and the presence and functional contribution o
13 taining was found in both the smooth muscle (detrusor) and urothelium layers of the urinary bladder.
14 cts of overactive sphincter afferents on the detrusor, and determination of the central nervous syste
15 der transient pressure events, whole bladder detrusor Ca(2+) activity and single UBSM ion channel act
16 xpressions of TGF-beta1 and CTGF in cultured detrusor cells of pBOO rats were increased but were impr
17                          Knockout of Ogg1 in detrusor cells resulted in accumulation of reactive oxyg
18 ic knock-out of Ogg1 in as few as 10% of the detrusor cells tripled the proliferation of the remainin
19             TRPV4 may also directly regulate detrusor contractility and the urothelial barrier functi
20                     There were no changes in detrusor contractility between the groups.
21 ulation has an indirect modulatory effect on detrusor contractility rather than a direct effect on th
22 ractivity and a smaller number have impaired detrusor contractility, sensory urgency, sphincteric inc
23 t had no effect on bladder wall mechanics or detrusor contractility.
24        Mechanisms responsible for regulating detrusor contraction during filling are poorly understoo
25          How magnetic stimulation suppresses detrusor contraction is not known.
26 ceptor stimulation produces the main part of detrusor contraction.
27 and in forming the input limb to involuntary detrusor contractions in neurogenic and probably also no
28  evaluation at 8 weeks after SCI showed that detrusor contractions of the bladder recovered similarly
29 ) can result from an interaction of unstable detrusor contractions, delayed arousal from sleep, and n
30 ation of reflex micturition, with associated detrusor contractions, resulted in voiding in a signific
31 ization of PDGFRalpha(+) cells and decreased detrusor contractions.
32 ited currents activated by GSK and increased detrusor contractions.
33  has a role beyond its known contribution to detrusor contractions.
34   The present study examined whether bladder detrusor dysfunction due to partial bladder outlet obstr
35 howed hAFSCs treatment could improve bladder detrusor dysfunction in pBOO rats, which may be related
36  bladder smooth muscle (UBSM) comprising the detrusor elicit transient non-voiding pressure events an
37  results show that the extent of recovery of detrusor-EUS coordination depends on injury severity and
38 verely injured rats, the chronic recovery of detrusor-EUS coordination was very incomplete and correl
39  at the injury site and complete recovery of detrusor-EUS coordination.
40  residual supraspinal connections on chronic detrusor-EUS coordination.
41 mast cell activator compound 48/80 increased detrusor excitability and bladder wall mechanical compli
42                         While the effects on detrusor excitability depended on urothelial prostagland
43 ere we describe a novel pathway to stabilize detrusor excitability involving platelet-derived growth
44 amin-sensitive stabilizing factor regulating detrusor excitability is likely to be due to the express
45 propria (LP) activate mechanisms controlling detrusor excitability.
46 4 channels during bladder filling stabilizes detrusor excitability.
47 ese cells might participate in regulation of detrusor excitability.
48                       Bladder smooth muscle (detrusor) exhibits spontaneous rhythmic activity (tone)
49 phosphamide-induced bladder inflammation and detrusor expansion.
50                                     Although detrusor expresses the S1P receptors S1P1 and S1P2, only
51                                              Detrusor-external sphincter dyssynergia (DSD) is a commo
52 ies have demonstrated age-related changes in detrusor function and urothelial transmitter release but
53                 Physiological examination of detrusor function in vitro using isolated bladder strips
54        We conclude that sexual dimorphism of detrusor function is prominent in rhesus macaques, share
55                                              Detrusor function was investigated by filling cystometry
56 le out baseline retention suggestive of poor detrusor function, and patients should be kept under car
57 rostatic surgery by providing information on detrusor function; and non-invasive urodynamic technique
58 nger intercontractile intervals (P<0.05) and detrusor hyperactivity (3-fold more prevoid contractions
59  formation of the NLRP3 complex resulting in detrusor hyperplasia.
60 d micturition pressure and fewer episodes of detrusor hyperreflexia.
61                           Some bladders with detrusor hypertrophy function close to normal (compensat
62  of decompensated bladders to empty, despite detrusor hypertrophy, is associated with an overexpressi
63 trast, older animals with diabetes exhibited detrusor hypoactivity, findings consistent with clinical
64 rease in the number of CARTp-IR cells in rat detrusor in early postnatal development; 2) apoptotic ev
65                 In children with NE and DVS, detrusor instability may play a major role in the causat
66 c, conservative therapies aimed at resolving detrusor instability or bladder outlet obstruction.
67 anical bladder outlet obstruction may induce detrusor instability with subsequent obstructed/overacti
68 ment for neuropathic bladder dysfunction and detrusor instability.
69 s, increase bladder compliance, and decrease detrusor instability.
70                          Overactivity in the detrusor is a common clinical problem.
71 ctivity for c-kit was detected in mucosa and detrusor layers of pig bladder.
72  ICs, was investigated in the mucosa and the detrusor layers of the pig bladder.
73 uption of SHH signaling, a known mediator of detrusor morphogenesis.
74 -labeling, was up-regulated in fetal bladder detrusor muscle and lamina propria cells and that this w
75                   Three types existed in the detrusor muscle and one major type in the sub-urothelium
76 re was reduced birefringent collagen between detrusor muscle bundles, and atomic force microscopy sho
77  of inflammatory and pro-fibrotic markers in detrusor muscle cells.
78 d PDGFRalpha and SK3 protein were reduced in detrusor muscle extracts.
79 ammation, increased mast cell numbers in the detrusor muscle have been reported in a subset of IC pat
80 eflexively increases activity of the bladder detrusor muscle in anesthetized rats.
81         The strong expression of PARs in the detrusor muscle indicates the need for studies on the ro
82 rative histopathological findings to confirm detrusor muscle infiltration.
83 ccount of this evidence, we propose that the detrusor muscle is arranged into modules, which are circ
84             Our results demonstrate that the detrusor muscle is hyperactive, voiding volume is decrea
85 early-stage cancer without invasion into the detrusor muscle layer.
86 ooth muscle cells (SMCs) in vitro and in the detrusor muscle of a mechanically overloaded bladder in
87 c component of neurotransmission in isolated detrusor muscle of guinea pig urinary bladder.
88 s assumption by studying E-C coupling in the detrusor muscle of wild type and Homer1(-/-) mice and by
89 al recording from smooth muscle cells of the detrusor muscle revealed spontaneous depolarizations, di
90 omplished by suppressing contractions of the detrusor muscle that lines the bladder wall.
91 ls subjacent to the epithelium and a thinner detrusor muscle that was not attributable to disruption
92 as associated with higher sensitivity of the detrusor muscle to muscarinic stimulation and membrane d
93                   S1P-induced contraction of detrusor muscle was dependent on stretch and intracellul
94           Most nerve endings were located in detrusor muscle where the three types could be identifie
95 he hypogastric (presumably inhibitory to the detrusor muscle).
96 e pelvic nerve (presumably excitatory to the detrusor muscle); and a pathway involving the pelvic ner
97 ereas PAR-1 and PAR-2 are predominant in the detrusor muscle, and PAR-4 is expressed in peripheral ne
98             Treatment for overactive bladder detrusor muscle, including anticholinergics (eg, trospiu
99 loss of coordinated neural control among the detrusor muscle, which increases bladder pressure to fac
100  an explanation for purinergic relaxation in detrusor muscles and show that there are no discrete inh
101 eported a new class of interstitial cells in detrusor muscles and showed that these cells could be id
102 mooth muscle cells (SMCs) were isolated from detrusor muscles of PDGFRalpha(+)/eGFP and smMHC/Cre/eGF
103 matory markers were increased in CYP-treated detrusor muscles.
104 el mechanism involving interstitial cells in detrusor muscles.
105 ient contraction and prolonged relaxation of detrusor muscles.
106         Experiments used isolated guinea-pig detrusor myocytes and store Ca(2+) content was estimated
107 fold increase in the cross-sectional area of detrusor myocytes following PBOO in male New Zealand Whi
108 iological studies using isolated rat bladder detrusor myocytes have demonstrated that compound 79 pro
109 re performed in wholemounts of urothelium or detrusor or cryostat sections of the bladder.
110 re usually caused by BPH, overactive bladder detrusor, or both.
111  injury (SCI)-induced bladder dysfunction is detrusor overactivity (DO).
112 he cystitis occurring in patients, including detrusor overactivity (DO).
113                                   Neurogenic detrusor overactivity (NDO) is a well known consequence
114                                   Neurogenic detrusor overactivity (NDO) is among the most challengin
115  multiple sclerosis often develop neurogenic detrusor overactivity (NDO), which currently lacks a uni
116                      Approximately half have detrusor overactivity and a smaller number have impaired
117 se results suggest that constipation induced detrusor overactivity and increased excitatory serotonin
118  established in the management of refractory detrusor overactivity and overactive bladder.
119 urrent therapeutic alternatives for managing detrusor overactivity and possible future developments a
120 wn to increase cystometric capacity, inhibit detrusor overactivity and resolve overactive bladder sym
121  treatment, both in patients with neurogenic detrusor overactivity and those with idiopathic detrusor
122 nary incontinence, overflow incontinence and detrusor overactivity are the major categories of urinar
123            Bladders of DKO animals exhibited detrusor overactivity at an early stage: increased frequ
124 mechanism that prostatic inflammation causes detrusor overactivity by using a rat model of chemically
125 abetic bladder dysfunction, characterized by detrusor overactivity during the early stage of the dise
126 veloped LUTS including urinary frequency and detrusor overactivity evaluated by awake cystometry.
127                                              Detrusor overactivity is a relatively common yet embarra
128  in our understanding of the pathogenesis of detrusor overactivity is slow but steady.
129                                              Detrusor overactivity is the occurrence of abnormal incr
130 onventional treatments like drug therapy for detrusor overactivity or sling procedures for female str
131                                              Detrusor overactivity poses a major challenge to physici
132 tract dysfunction, especially for those with detrusor overactivity refractory to anticholinergics, is
133                              We propose that detrusor overactivity results from exaggerated symptomat
134 ts acting on alternative pathways underlying detrusor overactivity with the intention of improving st
135 ive in reducing incontinence associated with detrusor overactivity, and repeated treatments appear sa
136 with pressure-flow urodynamics demonstrating detrusor overactivity, in the setting of a clinically re
137 r hypersensitivity as well as non-neurogenic detrusor overactivity, there is up-regulation of unmyeli
138  neurogenic and probably also non-neurogenic detrusor overactivity.
139  by targeting alternative pathways affecting detrusor overactivity.
140 guidelines recommend urodynamics to identify detrusor overactivity.
141 ave transformed the management of neurogenic detrusor overactivity.
142 accuracy compared to urodynamically-observed detrusor overactivity.
143 act symptoms/overactive bladder syndrome/and detrusor overactivity.
144 rusor overactivity and those with idiopathic detrusor overactivity.
145 gaining importance in the pathophysiology of detrusor overactivity.
146 l PDGFRalpha(+) cells are more abundant than detrusor PDGFRalpha(+) cells and express higher levels o
147 d that suburothelial PDGFRalpha(+) cells and detrusor PDGFRalpha(+) cells display different gene expr
148 es, which diagnose obstruction by evaluating detrusor pressure and flow rate during voiding.
149                                 However, the detrusor pressure during the lengthened ICI (i.e., urina
150 ed to significantly reduced aberrant maximum detrusor pressure during voiding and a reduction of the
151 function have shown improvements in storage, detrusor pressure, and emptying.
152                             IL-1beta-induced detrusor proliferation and hypertrophy could be reversed
153  rheumatoid arthritis therapeutic, prevented detrusor proliferation in conditioned media experiments
154 be a useful marker to estimate the degree of detrusor remodeling and contractile dysfunction in PBOO.
155 orded potent KCOs that possessed the desired detrusor selectivity when administered orally.
156   Inhibition of TREK-1 channels in the human detrusor significantly delayed relaxation of the stretch
157 hesis that NDO is associated with changes in detrusor smooth muscle (DSM) large conductance Ca(2+)-ac
158 udy was to develop a decentralized (ex vivo) detrusor smooth muscle (DSM)-denuded mouse bladder prepa
159       While Hpse2 is largely dispensable for detrusor smooth muscle and urothelial cell fate determin
160 ied higher levels of expression of TREK-1 in detrusor smooth muscle cells in comparison to bladder mu
161 he transient rise of intracellular Ca(2+) in detrusor smooth muscle cells is due to the release of Ca
162      We speculate that enhanced apoptosis in detrusor smooth muscle cells is part of a remodeling res
163 stimulation were examined on preparations of detrusor smooth muscle from guinea-pig urinary bladder u
164 lso a feature of differentiated vascular and detrusor smooth muscle in the bladder.
165 thral walls contract at the same time as the detrusor smooth muscle in the body of the bladder.
166 on-induced expression of TNC and CTGF in the detrusor smooth muscle of bladders from wild-type mice w
167 ession was also detected in the vascular and detrusor smooth muscle of the human bladder.
168 sine-1-phosphate (S1P), in regulating rabbit detrusor smooth muscle tone and contraction.
169 ur results demonstrate that S1P may regulate detrusor smooth muscle tone and suggest that dysregulati
170  Impaired neurogenic contractility of mutant detrusor smooth muscle was also significantly improved.
171 natal day [P]1, P3), CARTp-IR cell bodies in detrusor smooth muscle were observed in large clusters (
172 ut the bladder, including the urothelium and detrusor smooth muscle.
173  but may also be localized in subepithelium, detrusor smooth muscles and afferent neurons.
174                        Four weeks after SCI, detrusor sphincter dyssynergia had developed in all untr
175                                              Detrusor sphincter dyssynergia is a potentially life-thr
176 wer urinary tract dysfunction, in particular detrusor sphincter dyssynergia.
177 injuries (SCIs), patients may develop either detrusor-sphincter dyssynergia (DSD) or urinary incontin
178 l sphincter, a pattern necessary to overcome detrusor-sphincter dyssynergia.
179 ile 1 in the relaxation of precontracted rat detrusor strips can also be obtained with cyanobenzylami
180 adders demonstrated basal PCs whilst denuded-detrusor strips did not.
181                                              Detrusor strips from 5-HT3Avs/vs mice failed to contract
182 ic contractions (PCs) in mucosal and denuded-detrusor strips from juvenile and adult pigs were assess
183 duced PCs of both juvenile and adult denuded-detrusor strips, although strips from juvenile bladders
184 tion was studied in vitro using isolated rat detrusor strips.
185 th muscle between the urothelium and bladder detrusor, termed the muscularis mucosa.
186                                              Detrusor tissue from these mice was used to identify two
187 rect evidence that the response of the human detrusor to mechanical stretch is regulated by activatio
188 ctility studies determined a decreased basal detrusor tone and reduced amplitude of nerve-mediated co
189                            Cystometry showed detrusor underactivity (DU) with increased bladder capac
190 UAB) can be used as a general term, covering detrusor underactivity as the urodynamic diagnosis, and
191 ty during the early stage of the disease and detrusor underactivity during the late stage, is a commo
192 rwent a urodynamic study, which demonstrated detrusor underactivity of the bladder in 7 patients.
193            These findings were suggestive of detrusor underactivity.
194  obstruction, and urinary retention owing to detrusor underactivity.
195 found that GFRalpha3-IR axons innervated the detrusor, vasculature, and urothelium, but only part of
196 ethral angle, intraprostatic protrusion, and detrusor wall thickness are used to find a noninvasive w
197 IR, but the noradrenergic innervation of the detrusor was GFRalpha3-negative.
198 channels in ICCs-DM were responsible for the detrusor weak contractility of Diabetic cystopathy (DCP)
199 on with intact urothelium and SubU/LP but no detrusor, which allows direct access to the SubU/LP surf

 
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