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Vol. 280, Issue 1, 154-161, 1997
Department of Experimental and Clinical Pharmacology, University of
Graz, Universitätsplatz 4, A-8010 Graz, Austria (P.H., I.Th.L.)
and
Department of Pharmacology, University Medical School Pécs
P.O.B. 99, H-7643 Pécs, Hungary (A.L.T., L.L., L.B.)
The implications of the enteric neurotransmitter nitric oxide (NO) in
intestinal peristalsis were investigated. Propulsive motility in
isolated segments of the guinea pig ileum was triggered by intraluminal
fluid infusion to distend the intestinal wall, and the pressure
threshold for eliciting peristaltic waves was used to quantify
facilitation (decrease in threshold) or inhibition (increase in
threshold) of peristalsis. The NO donor sodium nitroprusside (0.1-100
µM serosally) caused a prompt facilitation of peristalsis, which in
the presence of a threshold concentration of atropine (10 nM) was
followed by a concentration-related blockade of peristalsis. Further
analysis showed that sodium nitroprusside (10 and 100 µM) first
relaxed, then contracted, and finally relaxed the longitudinal muscle
of the guinea pig isolated ileum, the contraction being blocked by
atropine (1 µM). Inhibition of NO synthase by
NG-nitro-L-arginine methylester (100-300 µM)
facilitated peristalsis, an effect that was reduced by
L-arginine (1 mM) but left unaltered by atropine (10 nM).
Blockade of inhibitory neuromuscular transmission by successive
exposure of the ileum to apamin (0.5 µM) and
NG-nitro-L-arginine methylester (300 µM), in
this or reverse order, disrupted the coordinated pattern of peristalsis
and caused irregular nonpropulsive contractions of the circular muscle.
It is concluded that NO has a dual excitatory and inhibitory effect on
intestinal motility. The excitatory effect involves cholinergic motor
neurons, whereas the inhibitory effect reflects relaxation of
intestinal muscle. Abolition of peristalsis by combined exposure to
NG-nitro-L-arginine methylester and apamin
attests to an essential role of enteric inhibitory motor neurons in the
coordination of propulsive motility in the intestine.
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