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
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.