Pharmacological properties of non-adrenergic, non-cholinergic inhibitory transmission in chicken gizzard

Abstract

1. Non-adrenergic, non-cholinergic (NANC) inhibitory transmission in chicken gizzard was studied by use of intracellular microelectrode techniques. Changes in membrane potential in response to NANC nerve stimulation were recorded in the gizzard smooth muscle pretreated with atropine (1 μM) and guanethidine (1 μM). 2. Field stimulation of the intramural nerves (FS) evoked inhibitory junction potentials (i.j.ps) which were abolished by tetrodotoxin (1 μM), but not inhibited at all by K+ channel blockers including apamin (0.5 μM), tetraethylammonium (TEA, 10 mM), charybdotoxin (0.2 μM) and glibenclamide (10 μM). 3. N(G)-nitro-L-arginine (300 μM), an inhibitor of nitric oxide (NO) synthase, inhibited i.j.ps. The effect was reversed by L-arginine (3 mM), but not by D-arginine (3 mM). 4. 8-Bromo cyclic GMP (100 μM), a membrane permeable analogue of cyclic GMP, produced a membrane hyperpolarization which was blocked by TEA (10 mM) or glibenclamide (10 μM). 5. NO at concentrations of up to 400 μM affected neither i.j.ps nor resting membrane potential. On the other hand, NO (80 μM) caused the membrane to hyperpolarize in the smooth muscle of guinea-pig ileum. 6. These results suggest that in the chicken gizzard, NANC i.j.ps may not arise from opening of conventional types of K+ channel and that NO seems unlikely to be involved in the generation of i.j.ps. A possible mechanism by which the inhibitory effect of N(G)-nitro-L-arginine on i.j.ps was brought about will be discussed.