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Inhibitory Effect and Possible Mechanism of Intraurethral Stimulation on Overactive Bladder in Female Rats.

Tian Y, Liao L, Wyndaele JJ - Int Neurourol J (2015)

Bottom Line: Cystometry was performed in 13 urethane-anesthetized female rats.Infusion of acetic acid significantly decreased bladder capacity.Activation of urethral afferent nerves can reverse OAB, which activates C-fiber afferent nerves.

View Article: PubMed Central - PubMed

Affiliation: Department Translational Neurosciences, Laboratory Urology, University of Antwerp, Faculty GGW, Antwerp, Belgium ; Department of Urology, University Hospital Antwerp, Antwerp, Belgium ; Department of Urology, China Rehabilitation Research Center, Capital Medical University, Beijing, China.

ABSTRACT

Purpose: To investigate the inhibitory effect and possible mechanism of intraurethral stimulation on overactive bladder (OAB) induced by acetic acid irritation.

Methods: Cystometry was performed in 13 urethane-anesthetized female rats. Intravesical infusion of 0.5% acetic acid was used to irritate the bladder and induce OAB. Multiple cystometrograms were performed with mirabegron, continuous stimulation, mirabegron plus continuous stimulation, and β3-adrenoceptor antagonist plus continuous stimulation to determine the mechanism underlying the inhibitory effect by intraurethral stimulation.

Results: Infusion of acetic acid significantly decreased bladder capacity. Intraurethral stimulation at 2.5 Hz plus mirabegron significantly increased bladder capacity and decreased the nonvoiding contraction count. The changes were strongly inhibited after the β3-adrenoceptor antagonist was administered.

Conclusions: Activation of urethral afferent nerves can reverse OAB, which activates C-fiber afferent nerves. This animal study indicates that intraurethral stimulation may interfere with OAB through hypogastric nerve activation and pudendal nerve neuromodulation.

No MeSH data available.


Related in: MedlinePlus

Results with infusion of saline, acetic acid (AA), mirabegron, continuous stimulation (CS), mirabegron plus CS, L748337 plus CS, and AA. (A) mirabegron, CS, and mirabegron plus CS significantly increased bladder capacity (BC) after AA. (B) The BC of the mirabegron (P=0.005) and CS groups (P=0.003) was significantly increased. There was no significant difference in BC between the mirabegron and CS groups (P=0.964). (C) The maximum pressure of voiding contraction (MPC) increased after mirabegron (P=0.014). The MPC decreased in the L748337 plus CS group (P=0.004). (D) The MPC of the CS (P=0.947) and mirabegron plus CS (P=0.980) groups was not significantly different compared with AA. (E) The nonvoiding contraction (NVC) count per filling period in the mirabegron (P=0.003), CS (P=0.001), and mirabegron plus CS groups (P=0.008) was decreased. The NVC count was increased after L748337 (P=0.017). (F) The ability of mirabegron to inhibit NVC was more significant than that of CS (P=0.028). *P<0.05, statistically significant difference.
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f3-inj-19-3-151: Results with infusion of saline, acetic acid (AA), mirabegron, continuous stimulation (CS), mirabegron plus CS, L748337 plus CS, and AA. (A) mirabegron, CS, and mirabegron plus CS significantly increased bladder capacity (BC) after AA. (B) The BC of the mirabegron (P=0.005) and CS groups (P=0.003) was significantly increased. There was no significant difference in BC between the mirabegron and CS groups (P=0.964). (C) The maximum pressure of voiding contraction (MPC) increased after mirabegron (P=0.014). The MPC decreased in the L748337 plus CS group (P=0.004). (D) The MPC of the CS (P=0.947) and mirabegron plus CS (P=0.980) groups was not significantly different compared with AA. (E) The nonvoiding contraction (NVC) count per filling period in the mirabegron (P=0.003), CS (P=0.001), and mirabegron plus CS groups (P=0.008) was decreased. The NVC count was increased after L748337 (P=0.017). (F) The ability of mirabegron to inhibit NVC was more significant than that of CS (P=0.028). *P<0.05, statistically significant difference.

Mentions: The BC decreased to 28.0% (0.10±0.04 mL) of the saline control capacity (0.36±0.05 mL) after infusing 0.5% AA. Mirabegron, CS, and mirabegron plus CS significantly increased the BC to 174.2% ±27.9% (0.17 ±0.05 mL), 175.4% ±30.2% (0.17±0.04 mL), and 246.2%±46.7% (0.23±0.04 mL), respectively, of the AA control capacity (Figs. 2, 3A). The BC in the mirabegron plus CS group was significantly increased compared with that in the CS-alone group (P =0.006) (Fig. 3B). There was no significant difference in the BC between the mirabegron and CS groups (P=0.950) (Fig. 3B). Also, there was no significant difference between the L748337 plus CS group and the AA control group (P=0.294) (Fig. 3A).


Inhibitory Effect and Possible Mechanism of Intraurethral Stimulation on Overactive Bladder in Female Rats.

Tian Y, Liao L, Wyndaele JJ - Int Neurourol J (2015)

Results with infusion of saline, acetic acid (AA), mirabegron, continuous stimulation (CS), mirabegron plus CS, L748337 plus CS, and AA. (A) mirabegron, CS, and mirabegron plus CS significantly increased bladder capacity (BC) after AA. (B) The BC of the mirabegron (P=0.005) and CS groups (P=0.003) was significantly increased. There was no significant difference in BC between the mirabegron and CS groups (P=0.964). (C) The maximum pressure of voiding contraction (MPC) increased after mirabegron (P=0.014). The MPC decreased in the L748337 plus CS group (P=0.004). (D) The MPC of the CS (P=0.947) and mirabegron plus CS (P=0.980) groups was not significantly different compared with AA. (E) The nonvoiding contraction (NVC) count per filling period in the mirabegron (P=0.003), CS (P=0.001), and mirabegron plus CS groups (P=0.008) was decreased. The NVC count was increased after L748337 (P=0.017). (F) The ability of mirabegron to inhibit NVC was more significant than that of CS (P=0.028). *P<0.05, statistically significant difference.
© Copyright Policy
Related In: Results  -  Collection

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getmorefigures.php?uid=PMC4582086&req=5

f3-inj-19-3-151: Results with infusion of saline, acetic acid (AA), mirabegron, continuous stimulation (CS), mirabegron plus CS, L748337 plus CS, and AA. (A) mirabegron, CS, and mirabegron plus CS significantly increased bladder capacity (BC) after AA. (B) The BC of the mirabegron (P=0.005) and CS groups (P=0.003) was significantly increased. There was no significant difference in BC between the mirabegron and CS groups (P=0.964). (C) The maximum pressure of voiding contraction (MPC) increased after mirabegron (P=0.014). The MPC decreased in the L748337 plus CS group (P=0.004). (D) The MPC of the CS (P=0.947) and mirabegron plus CS (P=0.980) groups was not significantly different compared with AA. (E) The nonvoiding contraction (NVC) count per filling period in the mirabegron (P=0.003), CS (P=0.001), and mirabegron plus CS groups (P=0.008) was decreased. The NVC count was increased after L748337 (P=0.017). (F) The ability of mirabegron to inhibit NVC was more significant than that of CS (P=0.028). *P<0.05, statistically significant difference.
Mentions: The BC decreased to 28.0% (0.10±0.04 mL) of the saline control capacity (0.36±0.05 mL) after infusing 0.5% AA. Mirabegron, CS, and mirabegron plus CS significantly increased the BC to 174.2% ±27.9% (0.17 ±0.05 mL), 175.4% ±30.2% (0.17±0.04 mL), and 246.2%±46.7% (0.23±0.04 mL), respectively, of the AA control capacity (Figs. 2, 3A). The BC in the mirabegron plus CS group was significantly increased compared with that in the CS-alone group (P =0.006) (Fig. 3B). There was no significant difference in the BC between the mirabegron and CS groups (P=0.950) (Fig. 3B). Also, there was no significant difference between the L748337 plus CS group and the AA control group (P=0.294) (Fig. 3A).

Bottom Line: Cystometry was performed in 13 urethane-anesthetized female rats.Infusion of acetic acid significantly decreased bladder capacity.Activation of urethral afferent nerves can reverse OAB, which activates C-fiber afferent nerves.

View Article: PubMed Central - PubMed

Affiliation: Department Translational Neurosciences, Laboratory Urology, University of Antwerp, Faculty GGW, Antwerp, Belgium ; Department of Urology, University Hospital Antwerp, Antwerp, Belgium ; Department of Urology, China Rehabilitation Research Center, Capital Medical University, Beijing, China.

ABSTRACT

Purpose: To investigate the inhibitory effect and possible mechanism of intraurethral stimulation on overactive bladder (OAB) induced by acetic acid irritation.

Methods: Cystometry was performed in 13 urethane-anesthetized female rats. Intravesical infusion of 0.5% acetic acid was used to irritate the bladder and induce OAB. Multiple cystometrograms were performed with mirabegron, continuous stimulation, mirabegron plus continuous stimulation, and β3-adrenoceptor antagonist plus continuous stimulation to determine the mechanism underlying the inhibitory effect by intraurethral stimulation.

Results: Infusion of acetic acid significantly decreased bladder capacity. Intraurethral stimulation at 2.5 Hz plus mirabegron significantly increased bladder capacity and decreased the nonvoiding contraction count. The changes were strongly inhibited after the β3-adrenoceptor antagonist was administered.

Conclusions: Activation of urethral afferent nerves can reverse OAB, which activates C-fiber afferent nerves. This animal study indicates that intraurethral stimulation may interfere with OAB through hypogastric nerve activation and pudendal nerve neuromodulation.

No MeSH data available.


Related in: MedlinePlus