Submitted on July 9, 2007
Accepted on August 20, 2007
Changes in Urinary Bladder Smooth Muscle Function in Response to Colonic Inflammation
Renata Noronha1, Hamid I. Akbarali2, Anna Malykhina3, Robert Foreman3, and Beverley Greenwood-Van Meerveld4*
1 Oklahoma Center for Neuroscience, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma, United States
2 Pharmacology and Toxicology, Medical College of Virginia, Richmond, Virginia, United States
3 Physiology, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma, United States
4 Veterans Affairs Medical Center, Oklahoma City, Oklahoma, United States; Oklahoma Cener for Neuroscience, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma, United States; Physiology, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma, United States
* To whom correspondence should be addressed. E-mail: beverley-greenwood{at}ouhsc.edu.
Background and aims: Visceral organ cross-talk is suspected to contribute to multi-organ symptomatology found in conditions such as irritable bowel syndrome (IBS) and interstitial cystitis (IC). The goal of the present study was to investigate the short and long term effects of acute colitis on bladder detrusor muscle contractility. We hypothesize that inflammation of the colon leads to changes in bladder function via direct changes in detrusor smooth muscle contractility. Methods: Colonic inflammation was induced in male rats via an enema of trinitrobenzenesulfonic acid (TNBS) (50mg/kg, 0.5ml, 25%EtOH). Colitis was confirmed using gross morphology, histology and measurements of myeloperoxidase (MPO) activity. Saline-enema treated rats served as controls. Following 3, 15 and 30 days post enema, bladder detrusor muscle contractility was investigated in response to electrical field stimulation (EFS), cholinergic agonism with carbachol (CCh) and potassium chloride (KCl). Results: During active colonic inflammation (day 3 post TNBS-enema), the bladder detrusor muscle appeared normal and showed no significant inflammation. However, abnormalities in bladder detrusor muscle contractility occurred in response to EFS and CCh but not KCl. During and following recovery from colonic inflammation (day 15 and 30 post-TNBS enema), changes in bladder detrusor muscle contractility in response to EFS and CCh returned to control levels. Conclusion: A transient colonic inflammatory insult significantly attenuates the amplitude of bladder detrusor muscle contractions in vitro, at least in part, through changes in cholinergic innervation that are reversible following recovery from the colitis.
