Nitric oxide modulates release of noradrenaline in guinea-pig gastric fundus.

The interaction between nitric oxide (NO) and the release of [(3)H]noradrenaline ([(3)H]NA) in conditions of non-activated and activated nicotinic receptors in guinea-pig gastric fundus preincubated with [(3)H]NA was studied. Nicotinic receptor agonist, 1,1-dimethyl-4-phenyl-piperazinium iodide (DMPP) (100 microM) significantly increased the resting release of [(3)H]NA. NO-synthase inhibitor, N(omega)-nitro-L-arginine (L-NNA) (100 microM) significantly decreased DMPP-induced release of [(3)H]NA. Field electrical stimulation (FES) (2Hz; 1 ms; 360 st) significantly increased the release of [(3)H]NA above the basal levels. L-NNA significantly decreased the stimulation-evoked release of [(3)H]NA. DMPP increased the stimulation-evoked release of [(3)H]NA, effect which was significantly decreased by L-NNA. The data suggests that endogenous NO increases the release of [(3)H]NA, evoked either by activation of the nicotinic receptors or by electrical stimulation in guinea-pig gastric fundus.