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1Institute of Medicine and 3Department of Physiology, College of Medicine, Chung-Shan Medical University, 5Division of Urology, Department of Surgery, and 6Division of Nephrology, Department of Internal Medicine, Taichung Veterans General Hospital, 2Department of Internal Medicine, Division of Nephrology, Taichung Armed General Hospital, 7Division of Neurosurgery, Department of Surgery, Chung-Shan Medical University Hospital and 4Department of Veterinary Medicine, College of Veterinary Medicine, Chung-Hsing University, Taichung, Taiwan
Submitted 5 July 2006 ; accepted in final form 16 October 2006
The effects of an acute increase in intraureteral pressure (IUP) on pelvic-urethra reflex potentiation were examined in urethane-anesthetized rats by recording the external urethral sphincter electromyogram activities evoked by the pelvic afferent stimulation. Compared with a single action potential elicited by the test stimulation (TS; characterized by an intensity that evoked a constant reflex response without facilitation, 1/30 Hz, 1.03 ± 0.12 spikes/stimulation, n = 7), the repetitive stimulation [RS; identical stimulation intensity as the TS (1 Hz)] significantly induced spinal reflex potentiation (SRP; 16.90 ± 2.00 spikes/stimulation, P < 0.01, n = 7). Such SRP was significantly attenuated by intrathecal 2,3-dihydroxy-6-nitro-7-sulfamoyl-benzo (F) quinoxaline [NBQX; a glutamatergic 
-amino-3-hydroxy-5-methyl-4-isoxazoleproprionat (AMPA) receptor antagonist] and D-2-amino-5-phosphonovalerate [APV; a glutamatergic N-methyl-D-aspartate (NMDA) antagonist; the spike number per stimulation: 11.0 ± 0.70 for NBQX, 1.01 ± 0.30 for APV, and 16.90 ± 2.0 for RS, respectively, n = 7, P < 0.01]. Acute stepwise elevations of IUP gradually attenuated and eventually abolished the RS-induced SRP (16.80 ± 1.30, 17.00 ± 1.30, 16.30 ± 1.30, 10.50 ± 1.80, 8.80 ± 1.90, 3.50 ± 1.60, 0.80 ± 0.20, 0.70 ± 0.20, and 0.20 ± 0.10 spikes/stimulation at intraureteral pressure of 0, 2.5, 5, 7.5, 10, 12.5, 15, 17.5, and 20 cmH2O, respectively, n = 7). Intrathecal NMDA (a glutamatergic NMDA receptor agonist) and bicuculline (a GABA receptor antagonist) both reversed the abolition of RS-induced SRP caused by unilateral ureteral distension (14.0 ± 4.04 and 8.00 ± 1.53 spikes/stimulation, respectively, n = 7, P < 0.01). All the results suggested unilateral ureteral distension might compensatorily relax the urethra via GABAergic inhibition of NMDA-dependent SRP.
intraureteral pressure; unilateral ureteral obstruction; spinal reflex potentiation; N-methyl-D-aspartic acid
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