{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,10,8]],"date-time":"2025-10-08T15:25:03Z","timestamp":1759937103907,"version":"3.37.3"},"reference-count":34,"publisher":"American Physiological Society","issue":"1","funder":[{"DOI":"10.13039\/100000062","name":"HHS | NIH | National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK)","doi-asserted-by":"publisher","award":["DK-094905","DK-102427","DK-091253"],"award-info":[{"award-number":["DK-094905","DK-102427","DK-091253"]}],"id":[{"id":"10.13039\/100000062","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2016,7,1]]},"abstract":"<jats:p> This study investigated the role of the hypogastric nerve and \u03b2-adrenergic mechanisms in the inhibition of nociceptive and non-nociceptive reflex bladder activity induced by pudendal nerve stimulation (PNS). In \u03b1-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 &lt; 0.01) increased bladder capacity to 184.7 \u00b1 12.6% and 214.5 \u00b1 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\u20133 mg\/kg iv) significantly ( P &lt; 0.05) reduced the inhibition. During AA irritation, the control bladder capacity was significantly ( P &lt; 0.05) reduced to \u223c22% of the saline control capacity. PNS at 2T and 4T significantly ( P &lt; 0.01) increased bladder capacity to 406.8 \u00b1 47% and 415.8 \u00b1 46% of the AA control capacity. Propranolol significantly ( P &lt; 0.05) reduced the bladder capacity to 276.3% \u00b1 53.2% (at 2T PNS) and 266.5 \u00b1 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 \u03b2-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. <\/jats:p>","DOI":"10.1152\/ajprenal.00180.2016","type":"journal-article","created":{"date-parts":[[2016,5,11]],"date-time":"2016-05-11T22:35:32Z","timestamp":1463006132000},"page":"F78-F84","source":"Crossref","is-referenced-by-count":18,"title":["Sympathetic \u03b2-adrenergic mechanism in pudendal inhibition of nociceptive and non-nociceptive reflex bladder activity"],"prefix":"10.1152","volume":"311","author":[{"given":"Brian T.","family":"Kadow","sequence":"first","affiliation":[{"name":"Department of Urology, University of Pittsburgh, Pittsburgh, Pennsylvania;"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Timothy D.","family":"Lyon","sequence":"additional","affiliation":[{"name":"Department of Urology, University of Pittsburgh, Pittsburgh, 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