TY - JOUR
T1 - Bladder overactivity induced by psychological stress in female mice is associated with enhanced bladder contractility
AU - West, Eliza
AU - Sellers, Donna J
AU - Chess-Williams, Russ
AU - McDermott, Catherine
PY - 2021/1/15
Y1 - 2021/1/15
N2 - Aims
To investigates the effects of water avoidance
stress on voiding behaviour and functional bladder responses in mice.
Main methods
Mice in the Stress group were exposed to water
avoidance stress (WAS) for 1 h/day for 10 days, Controls were age-matched and
housed normally. Voiding behaviour was measured periodically throughout the
stress protocol and bladders were isolated 24-h after final stress exposure to
measure bladder compliance, spontaneous phasic activity, contractile responses,
and release of urothelial mediators.
Key findings
Repeated stress exposure induced a significant
increase in plasma corticosterone levels in the WAS group compared to control.
An overactive bladder phenotype was observed in WAS mice, causing a significant
increase in the number of voiding events observed from as early as day-3, and a
7-fold increase following 10-days' stress. This increase in voiding frequency
was associated with a significant decrease in void size, an increase in the
number of small voids, but no change in total voided volume. Bladders from
stressed mice showed a significant increase in the maximum responses to the
muscarinic agonist carbachol (p < 0.01), in addition to enhanced pressure
responses to the purinergic agonists ATP (p < 0.05) and αβ-mATP (p <
0.05), and non-receptor mediated contractions to KCl (p < 0.05) compared to
controls. Nerve-mediated bladder contractions to electric field stimulation
were not significantly affected by stress, nor were spontaneous phasic
contractions or release of urothelial ATP and acetylcholine.
Significance
Repeated exposure to water avoidance stress
produced an overactive bladder phenotype, confirmed by increased voiding
frequency, and associated with enhanced bladder contractile responses.
AB - Aims
To investigates the effects of water avoidance
stress on voiding behaviour and functional bladder responses in mice.
Main methods
Mice in the Stress group were exposed to water
avoidance stress (WAS) for 1 h/day for 10 days, Controls were age-matched and
housed normally. Voiding behaviour was measured periodically throughout the
stress protocol and bladders were isolated 24-h after final stress exposure to
measure bladder compliance, spontaneous phasic activity, contractile responses,
and release of urothelial mediators.
Key findings
Repeated stress exposure induced a significant
increase in plasma corticosterone levels in the WAS group compared to control.
An overactive bladder phenotype was observed in WAS mice, causing a significant
increase in the number of voiding events observed from as early as day-3, and a
7-fold increase following 10-days' stress. This increase in voiding frequency
was associated with a significant decrease in void size, an increase in the
number of small voids, but no change in total voided volume. Bladders from
stressed mice showed a significant increase in the maximum responses to the
muscarinic agonist carbachol (p < 0.01), in addition to enhanced pressure
responses to the purinergic agonists ATP (p < 0.05) and αβ-mATP (p <
0.05), and non-receptor mediated contractions to KCl (p < 0.05) compared to
controls. Nerve-mediated bladder contractions to electric field stimulation
were not significantly affected by stress, nor were spontaneous phasic
contractions or release of urothelial ATP and acetylcholine.
Significance
Repeated exposure to water avoidance stress
produced an overactive bladder phenotype, confirmed by increased voiding
frequency, and associated with enhanced bladder contractile responses.
UR - http://www.scopus.com/inward/record.url?scp=85095946637&partnerID=8YFLogxK
U2 - 10.1016/j.lfs.2020.118735
DO - 10.1016/j.lfs.2020.118735
M3 - Article
C2 - 33166589
VL - 265
JO - Life sciences. Pt. 2: Biochemistry, general and molecular biology
JF - Life sciences. Pt. 2: Biochemistry, general and molecular biology
SN - 0024-3205
M1 - 118735
ER -