Abdominal muscle activity during voiding in female rats with normal or irritated bladder

Departments of 1 Pharmacology and 3 Urology, Faculty of Medicine, Dalhousie University, Halifax, Nova Scotia, Canada; and 2 Centro Tlaxcala de Biología de la Conducta, Universidad Autónoma de Tlaxcala, Tlaxcala, Mexico Submitted 28 July 2005 ; accepted in final form 20 December 2005 The aims of the present study were to determine in female rats whether abdominal muscle discharges during normal voiding and to describe the effect of bladder irritation on this visceromotor activity. The sensory pathway of this reflex was also determined. Electromyograms (EMGs) indicated that in awake rats, the abdominal muscle was consistently activated during spontaneous voiding and during voiding induced by saline infusion. Similarly, in anesthetized animals, the muscle discharged during urine expulsion. The abdominal EMG activity was not abolished by hypogastric (Hgnx) or sensory pudendal neurectomy (SPdnx). SPdnx dramatically decreased the intercontraction interval and voided volume. Acetic acid infusion reduced the intercontraction interval and increased bladder contraction duration. It also reduced the pressure threshold for evoking the abdominal EMG response and increased the EMG duration and amplitude. Although SPdnx and Hgnx modified some urodynamic parameters, they did not reverse the acetic acid effect on EMG activity. Thus the afferents activating the visceromotor reflex during normal voiding and the increased reflex in response to acetic acid are probably both carried by the pelvic nerve. Abdominal muscle activity induced by bladder distension has been considered to be a pain marker. However, we conclude that in female rats, the abdominal muscle is reflexively activated during physiological urine expulsion. On the other hand, bladder irritation is marked by an exaggeration of this abdominal visceromotor reflex. urethral sphincter; acetic acid; sensory pudendal nerve; hypogastric nerve Address for reprint requests and other correspondence: J. W. Downie, Dept. of Pharmacology, Faculty of Medicine, Sir Charles Tupper Medical Bldg., 5850 College St., Halifax, Nova Scotia, Canada B3H 1X5 (e-mail: john.downie{at}dal.ca )