Advanced

The role of corticotropin releasing factor and its antagonist, astressin, on micturition in the rat

Klausner, A P; Streng, Tomi LU ; Na, Y G; Raju, J; Batts, T W; Tuttle, J B; Andersson, Karl-Erik LU and Steers, W D (2005) In Autonomic Neuroscience: Basic & Clinical 123(1-2). p.26-35
Abstract
The purpose of this investigation was to evaluate the role of corticotropin releasing factor (CRF) on micturition. CRF is involved in the endocrine and central nervous system responses to stress and is also expressed in sites responsible for the control of micturition. In this investigation, cystometric experiments were performed in awake and unrestrained Wistar rats and on Spontaneous Hypertensive Rats, which are used as a rodent model of detrusor overactivity and anxiety. In vitro effects of CRF were evaluated using strips of detrusor muscle in an organ bath preparation. CRF (6.0 mu g) administered via intrathecal and intraperitoneal routes, but not intracerebroventricularly, lowered the micturition threshold. CRF reduced the... (More)
The purpose of this investigation was to evaluate the role of corticotropin releasing factor (CRF) on micturition. CRF is involved in the endocrine and central nervous system responses to stress and is also expressed in sites responsible for the control of micturition. In this investigation, cystometric experiments were performed in awake and unrestrained Wistar rats and on Spontaneous Hypertensive Rats, which are used as a rodent model of detrusor overactivity and anxiety. In vitro effects of CRF were evaluated using strips of detrusor muscle in an organ bath preparation. CRF (6.0 mu g) administered via intrathecal and intraperitoneal routes, but not intracerebroventricularly, lowered the micturition threshold. CRF reduced the intercontraction interval by 28% and 26% after intrathecal or intraperitoneal administration, respectively, and reduced micturition volume by 34.7% and 30.2%, respectively. In Wistar-Kyoto rats, 6.0 mu g intrathecal CRF significantly reduced intercontraction interval (423 +/- 79 vs. 669 +/- 59s) and micturition volume (0.30 +/- 0.04 vs. 0.69 +/- 0.07 ml) compared to controls that received saline vehicle. These effects were blocked by pretreatment with 6.0 mu g intrathecal astressin, a potent CRF antagonist, demonstrating that the effects are CRF receptor mediated. In Spontaneous Hypertensive Rats, 6.0 mu G intrathecal CRF was found to have minimal stimulatory effects on the bladder, whereas astressin reduced baseline detrusor overactivity. CRF had no direct contractile effects on detrusor muscle strips. These results demonstrate that in the absence of detrusor overactivity, CRE stimulates micturition when administered via the intrathecal or intraperitoneal routes. Further studies are needed to explore the possibility whether CRF antagonists are effective for detrusor overactivity and the overactive bladder syndrome. (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
rats, urination, corticotropin releasing factor, bladder, spontaneous, hypertensive rat
in
Autonomic Neuroscience: Basic & Clinical
volume
123
issue
1-2
pages
26 - 35
publisher
Elsevier
external identifiers
  • wos:000234166600004
  • pmid:16256445
  • scopus:28444433424
ISSN
1872-7484
DOI
10.1016/j.autneu.2005.08.003
language
English
LU publication?
yes
id
2ab9bb7a-9629-400b-9971-c8fad44c72aa (old id 210630)
date added to LUP
2007-09-28 12:01:59
date last changed
2017-09-17 04:30:36
@article{2ab9bb7a-9629-400b-9971-c8fad44c72aa,
  abstract     = {The purpose of this investigation was to evaluate the role of corticotropin releasing factor (CRF) on micturition. CRF is involved in the endocrine and central nervous system responses to stress and is also expressed in sites responsible for the control of micturition. In this investigation, cystometric experiments were performed in awake and unrestrained Wistar rats and on Spontaneous Hypertensive Rats, which are used as a rodent model of detrusor overactivity and anxiety. In vitro effects of CRF were evaluated using strips of detrusor muscle in an organ bath preparation. CRF (6.0 mu g) administered via intrathecal and intraperitoneal routes, but not intracerebroventricularly, lowered the micturition threshold. CRF reduced the intercontraction interval by 28% and 26% after intrathecal or intraperitoneal administration, respectively, and reduced micturition volume by 34.7% and 30.2%, respectively. In Wistar-Kyoto rats, 6.0 mu g intrathecal CRF significantly reduced intercontraction interval (423 +/- 79 vs. 669 +/- 59s) and micturition volume (0.30 +/- 0.04 vs. 0.69 +/- 0.07 ml) compared to controls that received saline vehicle. These effects were blocked by pretreatment with 6.0 mu g intrathecal astressin, a potent CRF antagonist, demonstrating that the effects are CRF receptor mediated. In Spontaneous Hypertensive Rats, 6.0 mu G intrathecal CRF was found to have minimal stimulatory effects on the bladder, whereas astressin reduced baseline detrusor overactivity. CRF had no direct contractile effects on detrusor muscle strips. These results demonstrate that in the absence of detrusor overactivity, CRE stimulates micturition when administered via the intrathecal or intraperitoneal routes. Further studies are needed to explore the possibility whether CRF antagonists are effective for detrusor overactivity and the overactive bladder syndrome.},
  author       = {Klausner, A P and Streng, Tomi and Na, Y G and Raju, J and Batts, T W and Tuttle, J B and Andersson, Karl-Erik and Steers, W D},
  issn         = {1872-7484},
  keyword      = {rats,urination,corticotropin releasing factor,bladder,spontaneous,hypertensive rat},
  language     = {eng},
  number       = {1-2},
  pages        = {26--35},
  publisher    = {Elsevier},
  series       = {Autonomic Neuroscience: Basic & Clinical},
  title        = {The role of corticotropin releasing factor and its antagonist, astressin, on micturition in the rat},
  url          = {http://dx.doi.org/10.1016/j.autneu.2005.08.003},
  volume       = {123},
  year         = {2005},
}