Abstract
Guinea-pig tracheal smooth muscle possesses an inhibitory non-adrenergic, non-cholinergic (i-NANC) innervation and the neurotransmitters involved in this response may be vasoactive intestinal peptide (VIP) and nitric oxide (NO). Since i-NANC mechanisms may co-exist with cholinergic nerves we have investigated whether endogenous VIP and NO modulate cholinergic neurotransmission. α-Chymotrypsin enhanced the cholinergic contractile responses to electrical field stimulation (EFS at 4 Hz by 38.6±4.8% (P < 0.05, n = 6) but did not produce a shift in the concentration-response curve to acetycholine (ACh). L-N G-Nitro-arginine methyl ester (L-NAME) and L-N G-monomethyl arginine (L-NMMA) produced a concentration-dependent enhancement of cholinergic responses to EFS (4 Hz) (at 100 μM, 40.9±6.6% and 30.2±5.8%, P < 0.01) with no effect on response curves to ACh. This enhancement was reversed by L-arginine but not D-arginine (1 mM). D-NAME and D-NMMA and L-arginine had no effect on cholinergic neurotransmission. α-Chymotrypsin and L-NAME had no effect on excitatory NANC (e-NANC) neural responses in guinea-pig bronchi. These results suggest that endogenous NO and VIP may modulate cholinergic neurotransmission by either functional antagonism at the level of the airway smooth muscle or via a pre-junctional inhibition of ACh release from cholinergic nerve terminals or by both mechanisms.
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