Changes in the composition of myosin isoforms in smooth muscle hypertrophy following urinary bladder outlet obstruction

2000 ◽  
pp. 81-100 ◽  
Author(s):  
Samuel K Chacko ◽  
Michael DiSanto ◽  
Yongmu Zheng ◽  
Alan J Wein
Keyword(s):  
Smooth Muscle ◽  
Urinary Bladder ◽  
Bladder Outlet Obstruction ◽  
Muscle Hypertrophy ◽  
Outlet Obstruction ◽  
Myosin Isoforms

REGIONAL ALTERATIONS IN THE EXPRESSION OF SMOOTH MUSCLE MYOSIN ISOFORMS IN RESPONSE TO PARTIAL BLADDER OUTLET OBSTRUCTION

2005 ◽  
Vol 173 (1) ◽  
pp. 302-308 ◽  
Author(s):  
ANITA S. MANNIKAROTTU ◽  
JOSEPH A. HYPOLITE ◽  
STEPHEN A. ZDERIC ◽  
ALAN J. WEIN ◽  
SAMUEL CHACKO ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Bladder Outlet Obstruction ◽  
Outlet Obstruction ◽  
Smooth Muscle Myosin ◽  
Myosin Isoforms ◽  
Partial Bladder Outlet Obstruction ◽  
Muscle Myosin

scholarly journals Leiomyoma of the seminal vesicle: a rare case

2013 ◽  
Vol 3 (2) ◽  
pp. 32 ◽  
Author(s):  
Aftab S. Shaikh ◽  
Girish D. Bakhshi ◽  
Arshad S. Khan ◽  
Nilofar M. Jamadar ◽  
Aravind Kotresh Nirmala ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Case Report ◽  
Urinary Bladder ◽  
Seminal Vesicle ◽  
Bladder Outlet Obstruction ◽  
Rare Case ◽  
Outlet Obstruction ◽  
Benign Tumors ◽  
Review Of Literature ◽  
Elderly Male

Leiomyomas though common benign tumors of smooth muscle cells are extremely rare in the male genitourinary tract. We present a case of an elderly male who presented with complaints suggestive of urinary bladder outlet obstruction since 1 year. His evaluation showed it due to a tumour arising from the left seminal vesicle. Excision of the tumor was done which was diagnosed on histopathology as leiomyoma. A brief case report and review of literature is being presented.

scholarly journals Calcineurin Mediates Bladder Smooth Muscle Hypertrophy After Bladder Outlet Obstruction

2003 ◽  
Vol 170 (5) ◽  
pp. 2077-2081 ◽  
Author(s):  
KUNIHIRO NOZAKI ◽  
KAZUHITO TOMIZAWA ◽  
TERUHIKO YOKOYAMA ◽  
HIROMI KUMON ◽  
HIDEKI MATSUI
Keyword(s):  
Smooth Muscle ◽  
Bladder Outlet Obstruction ◽  
Muscle Hypertrophy ◽  
Outlet Obstruction ◽  
Bladder Smooth Muscle

scholarly journals Smooth Muscle Hypertrophy Following Partial Bladder Outlet Obstruction Is Associated with Overexpression of Non-Muscle Caldesmon

2004 ◽  
Vol 164 (2) ◽  
pp. 601-612 ◽  
Author(s):  
Erik Y. Zhang ◽  
Raimund Stein ◽  
Shaohua Chang ◽  
Yongmu Zheng ◽  
Stephen A. Zderic ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Bladder Outlet Obstruction ◽  
Muscle Hypertrophy ◽  
Outlet Obstruction ◽  
Partial Bladder Outlet Obstruction

scholarly journals Bladder outlet obstruction triggers neural plasticity in sensory pathways and contributes to impaired sensitivity in erectile dysfunction

2013 ◽  
Vol 304 (10) ◽  
pp. R837-R845 ◽  
Author(s):  
Anna P. Malykhina ◽  
Qi Lei ◽  
Shaohua Chang ◽  
Xiao-Qing Pan ◽  
Antonio N. Villamor ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Erectile Dysfunction ◽  
Urinary Bladder ◽  
Bladder Neck ◽  
Bladder Outlet Obstruction ◽  
Corpus Cavernosum ◽  
Outlet Obstruction ◽  
Nerve Damage ◽  
Sensory Innervation ◽  
Sensory Neuropeptides

Lower urinary tract symptoms (LUTS) and erectile dysfunction (ED) are common problems in aging males worldwide. The objective of this work was to evaluate the effects of bladder neck nerve damage induced by partial bladder outlet obstruction (PBOO) on sensory innervation of the corpus cavernosum (CC) and CC smooth muscle (CCSM) using a rat model of PBOO induced by a partial ligation of the bladder neck. Retrograde labeling technique was used to label dorsal root ganglion (DRG) neurons that innervate the urinary bladder and CC. Contractility and relaxation of the CCSM was studied in vitro, and expression of nitric oxide synthase (NOS) was evaluated by Western blotting. Concentration of the sensory neuropeptides substance P (SP) and calcitonin gene-related peptide was measured by ELISA. Partial obstruction of the bladder neck caused a significant hypertrophy of the urinary bladders (2.5-fold increase at 2 wk). Analysis of L6-S2 DRG sections determined that sensory ganglia received input from both the urinary bladder and CC with 5–7% of all neurons double labeled from both organs. The contractile responses of CC muscle strips to KCl and phenylephrine were decreased after PBOO, followed by a reduced relaxation response to nitroprusside. A significant decrease in neuronal NOS expression, but not in endothelial NOS or protein kinase G (PKG-1), was detected in the CCSM of the obstructed animals. Additionally, PBOO caused some impairment to sensory nerves as evidenced by a fivefold downregulation of SP in the CC ( P ≤ 0.001). Our results provide evidence that PBOO leads to the impairment of bladder neck afferent innervation followed by a decrease in CCSM relaxation, downregulation of nNOS expression, and reduced content of sensory neuropeptides in the CC smooth muscle. These results suggest that nerve damage in PBOO may contribute to LUTS-ED comorbidity and trigger secondary changes in the contraction/relaxation mechanisms of CCSM.

1200: Alteration of Caveolae and Caveolins in Detrusor Smooth Muscle Hypertrophy Produced by Partial Bladder Outlet Obstruction

2005 ◽  
Vol 173 (4S) ◽  
pp. 325-326
Author(s):  
Erzsebet Polyak ◽  
Stephen A. Zderic ◽  
Anita Mannikarottu ◽  
Alan J. Wein ◽  
Samuel Chacko
Keyword(s):  
Smooth Muscle ◽  
Bladder Outlet Obstruction ◽  
Muscle Hypertrophy ◽  
Outlet Obstruction ◽  
Detrusor Smooth Muscle ◽  
Partial Bladder Outlet Obstruction

Reduction of endothelin-1 binding and inhibition of endothelin-1-mediated detrusor contraction by naftidrofuryl

2002 ◽  
Vol 103 (s2002) ◽  
pp. 459S-463S ◽  
Author(s):  
Robert C. CALVERT ◽  
Faiz H. MUMTAZ ◽  
Mick R. DASHWOOD ◽  
Masood A. KHAN ◽  
Robert J. MORGAN ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Urinary Bladder ◽  
Bladder Outlet Obstruction ◽  
Outlet Obstruction ◽  
Walking Distance ◽  
Receptor Subtype ◽  
Detrusor Muscle ◽  
Dependent Manner ◽  
Detrusor Contraction ◽  
Endothelin 1

Endothelin-1 (ET-1) causes urinary bladder smooth muscle contraction and the endothelin receptors A and B (ETA and ETB) are both known to be present in the rabbit urinary bladder. Alterations in ET-1 signalling have been implicated in the pathophysiology of urinary tract disorders secondary to bladder outlet obstruction and also in diabetic cystopathy. Naftidrofuryl (Naf) (marketed under the trade name Praxilene) improves walking distance in patients with peripheral vascular disease, an effect which may be partially attributed to ET-1 antagonism. The purpose of this study is to assess whether Naf will reduce ET-1 binding in the rabbit detrusor muscle and to assess whether there is inhibition of ET-1-mediated detrusor contraction. Detrusor smooth muscle strips were mounted in organ baths and cumulative response curves were measured for ET-1-mediated contractions in the presence and absence of 10-6M Naf (therapeutic concentration). In addition, ET-1 was added to the detrusor strips in the presence of the ETA antagonist, BQ123, and the ETB antagonist, BQ788, to identify the receptor subtype functionally involved. Overall inhibition of [125I]ET-1 binding by Naf was assessed using autoradiography. Identification of receptor-subtype binding reduction was assessed using the radioligands [125I]PD151242 and [125I]BQ3020. Naf inhibited ET-1-mediated detrusor contractions significantly (P<0.04), e.g. at 10-10M ET-1, contraction was completely abolished by Naf. Autoradiography indicated that Naf competitively inhibited [125I]ET-1 binding in a dose-dependent manner (IC50 = 3×10-7M). All radioligand binding was reduced indicating binding of Naf to both ETA and ETB receptors. Naf reduces binding of ET-1 to rabbit detrusor ETA and ETB receptors and inhibits ET-1-induced detrusor contractions mediated by ETA receptors. Naf may have therapeutic potential in the treatment of bladder disorders secondary to bladder outlet obstruction and diabetes mellitus.

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