Key result
Intraarterial labetalol reduces detrusor overactivity frequency by ~71% in hypertensive rats.
Why the study?
Patients with idiopathic overactive bladder may have autonomic nervous system dysfunction, particularly sympathetic dysfunction, but the detailed mechanisms are not well understood.
Does labetalol reduce detrusor overactivity in spontaneously hypertensive rats?
Does labetalol reduce detrusor overactivity in spontaneously hypertensive rats?
Absolute Event Rate: 0.28% vs 0.98%
p-value: p=<0.01
Nonselective sympathetic blockade with labetalol significantly reduces detrusor overactivity frequency and pressure in spontaneously hypertensive rats, suggesting a role for sympathetic modulation in overactive bladder.
Hypertensive rat model links ANS imbalance to detrusor overactivity; leaves open translation to human overactive bladder management.
The involuntary dual control systems of the autonomic nervous system (ANS) in the bladder of awake spontaneously hypertensive rats (SHRs) were investigated through simultaneous registrations of intravesical and intraabdominal pressures to observe detrusor overactivity (DO) objectively as a core symptom of an overactive bladder. SHRs (n = 6) showed the features of overactive bladder syndrome during urodynamic study, especially DO during the filling phase. After injection of the nonselective sympathetic blocking agent labetalol, DO disappeared in 3 of 6 SHRs (50%). DO frequency decreased from 0.98 ± 0.22 min(-1) to 0.28 ± 0.19 min(-1) (p < 0.01), and DO pressure decreased from 3.82 ± 0.57 cm H(2)O to 1.90 ± 0.86 cm H(2)O (p < 0.05). This suggests that the DO originating from the overactive parasympathetic nervous system is attenuated by the nonselective blocking of the sympathetic nervous system. The detailed mechanism behind this result is still not known, but parasympathetic overactivity seems to require overactive sympathetic nervous system activity in a kind of balance between these two systems. These findings are consistent with recent clinical findings suggesting that patients with idiopathic overactive bladder may have ANS dysfunction, particularly a sympathetic dysfunction. The search for newer and better drugs than the current anticholinergic drugs as the mainstay for overactive bladder will be fueled by our research on these sympathetic mechanisms. Further studies of this principle are required.
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Kim et al. (2012) studied Detrusor overactivity (n=12). Labetalol vs. Baseline (pre-injection) was evaluated on Detrusor overactivity (DO) frequency (events per minute) (p=<0.01). Intraarterial injection of labetalol in spontaneously hypertensive rats significantly decreased detrusor overactivity frequency from 0.98 to 0.28 per minute and pressure from 3.82 to 1.90 cm H2O.
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