This study investigated the role of the hypogastric nerve and β-adrenergic mechanisms in the inhibition of nociceptive and non-nociceptive reflex bladder activity induced by pudendal nerve stimulation (PNS). In α-chloralose-anesthetized cats, non-nociceptive reflex bladder activity was induced by slowly infusing saline into the bladder, whereas nociceptive reflex bladder activity was induced by replacing saline with 0.25% acetic acid (AA) to irritate the bladder. PNS was applied at multiple threshold (T) intensities for inducing anal sphincter twitching. During saline infusion, PNS at 2T and 4T significantly (P < 0.01) increased bladder capacity to 184.7 ± 12.6% and 214.5 ± 10.4% of the control capacity. Propranolol (3 mg/kg iv) had no effect on PNS inhibition, but 3-[(2-methyl-4-thiazolyl)ethynyl]pyridine (MTEP; 1-3 mg/kg iv) significantly (P < 0.05) reduced the inhibition. During AA irritation, the control bladder capacity was significantly (P < 0.05) reduced to ∼22% of the saline control capacity. PNS at 2T and 4T significantly (P < 0.01) increased bladder capacity to 406.8 ± 47% and 415.8 ± 46% of the AA control capacity. Propranolol significantly (P < 0.05) reduced the bladder capacity to 276.3% ± 53.2% (at 2T PNS) and 266.5 ± 72.4% (at 4T PNS) of the AA control capacity, whereas MTEP (a metabotropic glutamate 5 receptor antagonist) removed the residual PNS inhibition. Bilateral transection of the hypogastric nerves produced an effect similar to that produced by propranolol. This study indicates that hypogastric nerves and a β-adrenergic mechanism in the detrusor play an important role in PNS inhibition of nociceptive but not non-nociceptive reflex bladder activity. In addition to this peripheral mechanism, a central nervous system mechanism involving metabotropic glutamate 5 receptors also has a role in PNS inhibition.

Diagnosing urethral pathology can prove difficult, as clinically, the presentation is often nonspecific and may be suggestive of multiple etiologies. Therefore, detailed and accurate urethral imaging in both males and females is critical. Since the early 1900s, conventional imaging studies including RUG and VCUG, with adjunct cystourethroscopy, have remained the gold standard diagnostic techniques to evaluate urethral pathology. However, limitations of conventional imaging have generated interest in finding alternative imaging modalities with comparable, if not superior, diagnostic accuracy, the goal being a more complete assessment of urethral pathology and anatomy that would allow for appropriate surgical planning. Imaging modalities with three-dimensional (3D) capabilities may provide more comprehensive information regarding urethral diseases through a more detailed illustration of periurethral soft tissue structures. Whether or not these imaging modalities will replace conventional studies is unclear, though there is an increasing body of literature that support their use.

In a-chloralose anesthetized cats, we examined the role of opioid receptor (OR) subtypes (m, k, and d) in tibial nerve stimulation (TNS)-induced inhibition of bladder overactivity elicited by intravesical infusion of 0.25% acetic acid (AA). The sensitivity of TNS inhibition to cumulative i.v. doses of selective OR antagonists (cyprodime for m, nor-binaltorphimine for k, or naltrindole for d ORs) was tested. Naloxone (1 mg/kg, i.v., an antagonist for m, k, and d ORs) was administered at the end of each experiment. AA caused bladder overactivity and significantly (P , 0.01) reduced bladder capacity to 21.1% 6 2.6% of the saline control. TNS at 2 or 4 times threshold (T) intensity for inducing toe movement significantly (P , 0.01) restored bladder capacity to 52.9% 6 3.6% or 57.4% 6 4.6% of control, respectively. Cyprodime (0.3-1.0 mg/kg) completely removed TNS inhibition without changing AA control capacity. Nor-binaltorphimine (3-10 mg/kg) also completely reversed TNS inhibition and significantly (P , 0.05) increased AA control capacity. Naltrindole (1-10 mg/kg) reduced (P , 0.05) TNS inhibition but significantly (P , 0.05) increased AA control capacity. Naloxone (1 mg/kg) had no effect in cyprodime pretreated cats, but it reversed the nor-binaltorphimine-induced increase in bladder capacity and eliminated the TNS inhibition remaining in naltrindole pretreated cats. These results indicate a major role of m and k ORs in TNS inhibition, whereas d ORs play a minor role. Meanwhile, k and d ORs also have an excitatory role in irritation-induced bladder overactivity.