REFLEX PATHWAYS CONTROLLING URETHRAL STRIATED AND SMOOTH-MUSCLE FUNCTION IN THE MALE-RAT

Citation
H. Kakizaki et al., REFLEX PATHWAYS CONTROLLING URETHRAL STRIATED AND SMOOTH-MUSCLE FUNCTION IN THE MALE-RAT, American journal of physiology. Regulatory, integrative and comparative physiology, 41(5), 1997, pp. 1647-1656
Citations number
28
Categorie Soggetti
Physiology
ISSN journal
03636119
Volume
41
Issue
5
Year of publication
1997
Pages
1647 - 1656
Database
ISI
SICI code
0363-6119(1997)41:5<1647:RPCUSA>2.0.ZU;2-E
Abstract
The organization of vesicourethral reflex mechanisms in the male rat w as studied by monitoring intraurethral pressure and the external ureth ral sphincter (EUS) electromyogram. EUS striated and urethral smooth m uscle activities were elicited by reflex isovolumetric bladder contrac tions evoked by bladder filling or electrical stimulation of nerves in the bladder wall. Evoked EUS bursting activity in normal rats was eli minated in chronic spinal rats and replaced by tonic activity. Reflex urethral smooth muscle activity mediated by an increase in urethral pr essure after paralysis of the EUS with alpha-bungarotoxin occurred in normal and chronic spinal rats. The response was significantly larger in chronic spinal (21.3+/-3.0 cmH(2)O) than in normal rats (4.2+/-0.7 cmH(2)O). N-G-nitro-L-arginine methyl ester (a nitric oxide synthase i nhibitor, 20 mg/kg iv) increased the smooth muscle response in normal (5.9+/-1.3 cmH(2)O) and chronic spinal rats (6.9+/-1.8 cmH(2)O). This increase in urethral pressure was not changed by sympathetic nerve tra nsection or prazosin (0.2-0.3 mg/kg iv) but was abolished by hexametho nium and reduced 74-89% by atropine. These results indicate that coord inated EUS function (bursting activity) in the male rat is dependent o n supraspinal pathways and that the urethral smooth muscle response du ring voiding is composed of a predominant cholinergic, atropine-sensit ive contraction as well as a nitric oxide-mediated relaxation. Both ar e mediated by activation of parasympathetic pathways and are maintaine d or significantly larger after spinal cord injury, indicating that th ey are dependent on spinal reflex pathways.