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Treatment-resistant detrusor overactivity - underlying pharmacology and potential mechanisms.

Andersson, Karl-Erik LU orcid (2006) In International Journal of Clinical Practice Suppl 151(suppl. 151). p.8-16
Abstract
Bladder function during filling and micturition is regulated by peripheral and central nervous and hormonal control systems. Micturition occurs in response to afferent signals from the lower urinary tract, and distention of the bladder wall is the primary stimulus. In the animal and human bladder, efferent adrenergic, cholinergic and nonadrenergic, noncholinergic (NANC) neurotransmission has been demonstrated. The most important receptors for activation of contraction are muscarinic (M-3) and purinergic receptors (P2X(1)), however, the contribution of these receptors to contraction may differ between species, and may be changed in bladder dysfunction associated with detrusor overactivity (DO) and/or the overactive bladder (OAB) syndrome,... (More)
Bladder function during filling and micturition is regulated by peripheral and central nervous and hormonal control systems. Micturition occurs in response to afferent signals from the lower urinary tract, and distention of the bladder wall is the primary stimulus. In the animal and human bladder, efferent adrenergic, cholinergic and nonadrenergic, noncholinergic (NANC) neurotransmission has been demonstrated. The most important receptors for activation of contraction are muscarinic (M-3) and purinergic receptors (P2X(1)), however, the contribution of these receptors to contraction may differ between species, and may be changed in bladder dysfunction associated with detrusor overactivity (DO) and/or the overactive bladder (OAB) syndrome, such as outflow obstruction, neurogenic bladders, idiopathic DO and diabetes. The NANC component of the nerve-induced response in such disorders may be responsible for up to 40-50% of the total bladder contraction. Whether this in vitro'atropine-resistance' corresponds to DO/OAB seen in patients not responding to antimuscarinic treatment is not known. Afferent signalling from the urothelium may be involved in both normal bladder function and in DO/OAB, but its role in antimuscarinic-refractory patients remains to be established. Several central nervous system (CNS) transmitters/transmitter systems, including gamma aminobutyric acid (GABA), opioid, serotonin, noradrenaline, dopamine or glutamatergic receptors and mechanisms are known to be involved in micturition control. The contribution of these receptors and mechanisms in DO/OAB resistant to treatment with antimuscarinics is not known, but drugs acting at these sites may offer future treatment possibilities. (Less)
Please use this url to cite or link to this publication:
author
organization
publishing date
type
Contribution to journal
publication status
published
subject
keywords
urinary incontinence, detrusor contraction, afferent nerves
in
International Journal of Clinical Practice
volume
Suppl 151
issue
suppl. 151
pages
8 - 16
publisher
Wiley-Blackwell
external identifiers
  • wos:000242310000002
  • scopus:33751324838
ISSN
1742-1241
DOI
10.1111/j.1742-1241.2006.01184.x
language
English
LU publication?
yes
id
bffd3a84-48d5-417b-8313-0a5896b6e95f (old id 164006)
alternative location
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=17169005&dopt=Abstract
date added to LUP
2016-04-01 16:30:18
date last changed
2020-04-15 02:24:51
@article{bffd3a84-48d5-417b-8313-0a5896b6e95f,
  abstract     = {Bladder function during filling and micturition is regulated by peripheral and central nervous and hormonal control systems. Micturition occurs in response to afferent signals from the lower urinary tract, and distention of the bladder wall is the primary stimulus. In the animal and human bladder, efferent adrenergic, cholinergic and nonadrenergic, noncholinergic (NANC) neurotransmission has been demonstrated. The most important receptors for activation of contraction are muscarinic (M-3) and purinergic receptors (P2X(1)), however, the contribution of these receptors to contraction may differ between species, and may be changed in bladder dysfunction associated with detrusor overactivity (DO) and/or the overactive bladder (OAB) syndrome, such as outflow obstruction, neurogenic bladders, idiopathic DO and diabetes. The NANC component of the nerve-induced response in such disorders may be responsible for up to 40-50% of the total bladder contraction. Whether this in vitro'atropine-resistance' corresponds to DO/OAB seen in patients not responding to antimuscarinic treatment is not known. Afferent signalling from the urothelium may be involved in both normal bladder function and in DO/OAB, but its role in antimuscarinic-refractory patients remains to be established. Several central nervous system (CNS) transmitters/transmitter systems, including gamma aminobutyric acid (GABA), opioid, serotonin, noradrenaline, dopamine or glutamatergic receptors and mechanisms are known to be involved in micturition control. The contribution of these receptors and mechanisms in DO/OAB resistant to treatment with antimuscarinics is not known, but drugs acting at these sites may offer future treatment possibilities.},
  author       = {Andersson, Karl-Erik},
  issn         = {1742-1241},
  language     = {eng},
  number       = {suppl. 151},
  pages        = {8--16},
  publisher    = {Wiley-Blackwell},
  series       = {International Journal of Clinical Practice},
  title        = {Treatment-resistant detrusor overactivity - underlying pharmacology and potential mechanisms.},
  url          = {http://dx.doi.org/10.1111/j.1742-1241.2006.01184.x},
  doi          = {10.1111/j.1742-1241.2006.01184.x},
  volume       = {Suppl 151},
  year         = {2006},
}