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Vol. 283, Issue 1, 23-28, 1997
Department of Physiology and Neuroscience, Section of
Neuroendocrine CellBiology, University of Lund, Lund, Sweden
This study examines nitric oxide (NO) mediated effects on longitudinal
muscle with adherent myenteric ganglia from rat ileum in
vitro using NO donors and electrical field stimulation.
Electrical field stimulation (20 Hz) caused a biphasic response
a
relaxation followed by a contraction.
NG-nitro-L-arginine methyl ester almost totally
abolished the relaxation and L-arginine restored it. The
contraction was unaffected. The NO donors
sodium-nitroso-N-acetylpenicillamine (SNAP) and sodium-nitroprusside also induced a biphasic response, a contraction followed by relaxation. Relaxations mediated by neuronally released NO were not blocked by
methylene blue or 1H-[1,2,4]oxadiazolo[4,3-a]-quinoxalin-1-one suggesting that they are independent of a rise in intracellular cyclic
guanylate cyclase. Their amplitude was unaffected by forskolin. The
relaxations evoked by NO (or a NO-related substance) liberated from
SNAP were blocked by methylene blue or
1H-[1,2,4]oxadiazolo[4,3-a]-quinoxalin-1-one indicating a cyclic
guanylate cyclase-dependent mechanism of action. Pituitary adenylate
cyclase-activating peptide and forskolin, but not vasoactive intestinal
peptide or neuropeptide Y, caused a marked left-ward shift of the
concentration-response curve of the SNAP-induced relaxation. The
contractions induced by SNAP were blocked by methylene blue and
1H-[1,2,4]oxadiazolo[4,3-a]-quinoxalin-1-one and thus, cyclic
guanylate cyclase dependent. The SNAP-induced contractions were
abolished by pituitary adenylate cyclase-activating peptide and
forskolin, but unaffected by vasoactive intestinal peptide or NPY. In
conclusion, motor responses evoked by NO released from NO donors
vs. neuronally released NO reveals different mechanisms of action.
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