PMID- 21091642
OWN - NLM
STAT- MEDLINE
DCOM- 20110506
LR  - 20211020
IS  - 1476-5381 (Electronic)
IS  - 0007-1188 (Print)
IS  - 0007-1188 (Linking)
VI  - 162
IP  - 5
DP  - 2011 Mar
TI  - Biomechanical properties and innervation of the female caveolin-1-deficient 
      detrusor.
PG  - 1156-70
LID - 10.1111/j.1476-5381.2010.01115.x [doi]
AB  - BACKGROUND AND PURPOSE: Caveolin-1-deficiency is associated with substantial 
      urogenital alterations. Here, a mechanical, histological and biochemical 
      characterization of female detrusors from wild-type and caveolin-1-deficient (KO) 
      mice was made to increase the understanding of detrusor changes caused by lack of 
      caveolae. EXPERIMENTAL APPROACH: Length-tension relationships were generated, and 
      we recorded responses to electrical field stimulation, the muscarinic receptor 
      agonist carbachol and the purinoceptor agonist ATP. Tyrosine nitration and the 
      contents of caveolin-1, cavin-1, muscarinic M(3) receptors, phospholipase C(beta1), 
      muscle-specific kinase (MuSK) and L-type Ca(2+) channels were determined by 
      immunoblotting. Innervation was assessed by immunohistochemistry. KEY RESULTS: 
      Bladder to body weight ratio was not changed, nor was there any change in the 
      optimum circumference for force development. Depolarization- and ATP-induced 
      stress was reduced, as was carbachol-induced stress between 0.1 and 3 microM, but the 
      supramaximal relative (% K(+)) response to carbachol was increased, as was M(3) 
      expression. The scopolamine-sensitive component of the electrical field 
      stimulation response was impaired, and yet bladder nerves contained little 
      caveolin-1. The density of cholinergic nerves was unchanged, whereas CART- and 
      CGRP-positive nerves were reduced. Immunoblotting revealed loss of MuSK. 
      CONCLUSIONS AND IMPLICATIONS: Ablation of caveolae in the female detrusor leads 
      to generalized impairment of contractility, ruling out prostate hypertrophy as a 
      contributing factor. Cholinergic neuroeffector transmission is impaired without 
      conspicuous changes in the density of cholinergic nerves or morphology of their 
      terminals, but correlating with reduced expression of MuSK.
CI  - (c) 2011 The Authors. British Journal of Pharmacology (c) 2011 The British 
      Pharmacological Society.
FAU - Sadegh, Mardjaneh Karbalaei
AU  - Sadegh MK
AD  - Department of Experimental Medical Science, Lund University, Biomedical Centre, 
      Lund, Sweden.
FAU - Ekman, Mari
AU  - Ekman M
FAU - Rippe, Catarina
AU  - Rippe C
FAU - Sundler, Frank
AU  - Sundler F
FAU - Wierup, Nils
AU  - Wierup N
FAU - Mori, Michiko
AU  - Mori M
FAU - Uvelius, Bengt
AU  - Uvelius B
FAU - Sward, Karl
AU  - Sward K
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - England
TA  - Br J Pharmacol
JT  - British journal of pharmacology
JID - 7502536
RN  - 0 (Cav1 protein, mouse)
RN  - 0 (Caveolin 1)
RN  - 0 (DNA Primers)
RN  - 8L70Q75FXE (Adenosine Triphosphate)
RN  - 8Y164V895Y (Carbachol)
SB  - IM
MH  - Adenosine Triphosphate/pharmacology
MH  - Animals
MH  - Base Sequence
MH  - Biomechanical Phenomena
MH  - Carbachol/pharmacology
MH  - Caveolae/pathology/physiology
MH  - Caveolin 1/*deficiency/genetics/physiology
MH  - DNA Primers/genetics
MH  - Diuresis
MH  - Electric Stimulation
MH  - Female
MH  - Male
MH  - Mice
MH  - Mice, Congenic
MH  - Mice, Inbred C57BL
MH  - Mice, Knockout
MH  - Microscopy, Electron, Transmission
MH  - Muscle Contraction/drug effects
MH  - Muscle, Smooth/*innervation/pathology/*physiopathology
MH  - Organ Size
MH  - Prostatic Hyperplasia/complications
MH  - Synaptic Transmission
MH  - Urinary Bladder/innervation/pathology/physiopathology
MH  - Urinary Bladder Neck Obstruction/etiology/pathology/physiopathology
PMC - PMC3051387
EDAT- 2010/11/26 06:00
MHDA- 2011/05/07 06:00
PMCR- 2012/03/01
CRDT- 2010/11/25 06:00
PHST- 2010/11/25 06:00 [entrez]
PHST- 2010/11/26 06:00 [pubmed]
PHST- 2011/05/07 06:00 [medline]
PHST- 2012/03/01 00:00 [pmc-release]
AID - 10.1111/j.1476-5381.2010.01115.x [doi]
PST - ppublish
SO  - Br J Pharmacol. 2011 Mar;162(5):1156-70. doi: 10.1111/j.1476-5381.2010.01115.x.