The gut innervation is formed by an intrinsic and an extrinsic component. T
he former is responsible for the intestinal contractions that occur in the
total absence of extrinsic innervation. We hypothesize that the intrinsic p
lexuses do not produce local contraction, but mediate re? ex actions of the
gut musculature. This hypothesis was investigated in the rectum of the exp
erimental animal. In 16 anesthetized mongrel dogs, the rectum was exposed,
and 3 monopolar silver-silver chloride electrodes were sutured serially to
the rectal wall and connected to a rectilinear pen recorder. The rectal ele
ctric activity was recorded at rest and on rectal inflation while the anal
pressure was synchronously registered. The tests were repeated after separa
te drug administration using phentolamine, propranolol (adrenoceptor blocki
ng agents), atropine (cholinergic blocking agent), drotaverine (direct smoo
th muscle relaxant), and nitroglycerine. (NO donor, inhibitory noncholinerg
ic, nonadrenergic mediator). Slow waves or pacesetter potentials (PPs) and
action potentials (APs) were recorded from the three electrodes. Rectal bal
loon distension caused an increase of frequency, amplitude, and conduction
velocity of these waves, as well as a decrease of anal pressure. Repetition
of the test after administration of phentolamine, propranotol, and atropin
e effected no change in rectal electromyelographic (EMG) activity or anal p
ressure, while drotaverine and nitroglycerine administration aborted both t
he electric activity and the anal pressure response. We conclude that the r
ectal electric activity, presumably responsible for rectal motility, was no
t aborted by enteric nervous plexus block but by direct muscle relaxant. Th
is suggests that the enteric plexus has no direct action on the rectal moti
le activity but mediates the rectal reflex actions. This concept might expl
ain some of the hitherto unknown mechanisms of rectal dyssynergia syndromes
.