Effects of Intravesically Administered Anticholinergics, .BETA.-Adrenergic Stimulant and .ALPHA.-Adrenergic Blocker on Bladder Function in Unanesthetized Rats.

Ukimura, Osamu

doi:10.1620/tjem.170.251

Cited by 9 publications

(4 citation statements)

References 16 publications

(16 reference statements)

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“…Although similar increases in the micturition volume threshold following ␣-adrenergic block were reported in the decerebrate dog (35) and conscious rat (43), others have reported decreases in the micturition volume threshold in cats (16,18). One factor potentially responsible for these differences is peripheral (35,43) vs. central (18) drug administration (25). As well, the results may reflect variation in the ␣-adrenergic receptor subtypes, as intrathecal injection of prazosin increased the micturition volume threshold in rats (25) but had little effect in cats (18).…”

Section: Discussionsupporting

confidence: 72%

“…Blocking the ␣-adrenergic pathway with phentolamine increased the threshold volumes for distention-evoked and stimulation-evoked contractions. Although similar increases in the micturition volume threshold following ␣-adrenergic block were reported in the decerebrate dog (35) and conscious rat (43), others have reported decreases in the micturition volume threshold in cats (16,18). One factor potentially responsible for these differences is peripheral (35,43) vs. central (18) drug administration (25).…”

Section: Discussionmentioning

confidence: 62%

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Mechanisms of reflex bladder activation by pudendal afferents

Woock

Yoo

Grill

2011

American Journal of Physiology-Regulatory, Integrative and Comp

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Activation of pudendal afferents can evoke bladder contraction or relaxation dependent on the frequency of stimulation, but the mechanisms of reflex bladder excitation evoked by pudendal afferent stimulation are unknown. The objective of this study was to determine the contributions of sympathetic and parasympathetic mechanisms to bladder contractions evoked by stimulation of the dorsal nerve of the penis (DNP) in ␣-chloralose anesthetized adult male cats. Bladder contractions were evoked by DNP stimulation only above a bladder volume threshold equal to 73 Ϯ 12% of the distension-evoked reflex contraction volume threshold. Bilateral hypogastric nerve transection (to eliminate sympathetic innervation of the bladder) or administration of propranolol (a ␤-adrenergic antagonist) decreased the stimulation-evoked and distensionevoked volume thresholds by Ϫ25% to Ϫ39%. Neither hypogastric nerve transection nor propranolol affected contraction magnitude, and robust bladder contractions were still evoked by stimulation at volume thresholds below the distension-evoked volume threshold. As well, inhibition of distention-evoked reflex bladder contractions by 10 Hz stimulation of the DNP was preserved following bilateral hypogastric nerve transection. Administration of phentolamine (an ␣-adrenergic antagonist) increased stimulation-evoked and distension-evoked volume thresholds by 18%, but again, robust contractions were still evoked by stimulation at volumes below the distension-evoked threshold. These results indicate that sympathetic mechanisms contribute to establishing the volume dependence of reflex contractions but are not critical to the excitatory pudendal to bladder reflex. A strong correlation between the magnitude of stimulation-evoked bladder contractions and bladder volume supports that convergence of pelvic afferents and pudendal afferents is responsible for bladder excitation evoked by pudendal afferents. Further, abolition of stimulationevoked bladder contractions following administration of hexamethonium bromide confirmed that contractions were generated by pelvic efferent activation via the pelvic ganglion. These findings indicate that pudendal afferent stimulation evokes bladder contractions through convergence with pelvic afferents to increase pelvic efferent activity.cat; micturition; parasympathetic; sympathetic DEPENDING ON THE STIMULATION frequency, electrical stimulation of pudendal afferents evokes spinal reflexes that either inhibit the bladder and promote continence or excite the bladder and cause micturition in both cats (5,6,41,45,49) and persons with spinal cord injury (48). Previous results suggest that bladder inhibition by pudendal afferent stimulation arises from activation of hypogastric efferents and subsequent synaptic and ganglionic inhibition of parasympathetic efferents (8, 30), but the mechanisms of bladder excitation by pudendal afferent stimulation are not known. Contraction of the bladder by pudendal afferent stimulation may result from activation of a vestigial reflex from perig...

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Section: Discussionsupporting

confidence: 72%

Section: Discussionmentioning

confidence: 62%

Mechanisms of reflex bladder activation by pudendal afferents

Woock

Yoo

Grill

2011

American Journal of Physiology-Regulatory, Integrative and Comp

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“…There are several studies on the effectiveness of intravesical oxybutynin and capsaicin, but there is a paucity of literature on the effects of intravesical propantheline. Beneficial effects of intravesical propantheline in experimental animals have been reported [17,18,19].…”

Section: Discussionmentioning

confidence: 98%

The Effectiveness of Intravesical Oxybutynin, Propantheline, and Capsaicin in the Management of Neuropathic Bladder following Spinal Cord Injury

George

Tharion

Richar

et al. 2007

The Scientific World JOURNAL

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The objective of this study was to compare the therapeutic response of intravesical oxybutynin, propantheline, and capsaicin in the treatment of neurogenic detrusor overactivity. Carried out in the Department of Physical Medicine and Rehabilitation at a university teaching hospital in India, patients acted as their own controls. Oxybutynin 5 mg in solution or propantheline 15 mg in solution and capsaicin were instilled intravesically in each patient. Urodynamic studies were done before and after the intravesical instillation of each drug. The nonparametric tests were used for statistical analysis. The efficacy of intravesical capsaicin in the treatment of neurogenic detrusor overactivity was statistically significant for reflex volume (RV) (p = 0.018), cystometric capacity (CC) (p = 0.0440), leak volume (LV) (p = 0.000), and leak frequency (LF) (p = 0.009). The Kruskal-Wallis test for paired sample comparing pre- and post-LV and LF for intravesical capsaicin was significant at 2nd week (p = 0.002 and 0.054, respectively). There was a significant difference in therapeutic response between intravesical oxybutynin, propantheline, and capsaicin in the treatment of detrusor overactivity for LV and LF at 2nd week (p = 0.017 and 0.003, respectively). When comparing responses of oxybutynin and propantheline, more subjects demonstrated improvement with intravesical propantheline than oxybutynin for RV, detrusor leak point pressure (LPP), clean intermittent catheterization volume (CICV), and LV. This study suggests that intravesical agents may be used as effective adjuvants in the management of incontinence due to neurogenic detrusor overactivity following spinal cord injury.

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“…it has a direct relaxant effect on the smooth muscle of the urinary bladder [36]. Oxybutynin reduces both spontaneous and electrically induced contractions of the bladder [5,37]. The direct smooth muscle‐relaxant effect of oxybutynin is mediated by calcium antagonism.…”

Section: Intravesical Administration Of Oxybutyninmentioning

confidence: 99%