Venous relaxation caused by acetylcholine acting on the sympathetic nerves.

Experiments were performed to determine whether acetylcholine affects the sympathetic activation of the cutaneous veins of the dog. Changes in isometric tension of saphenous vein strips were recorded at 37°C in an organ bath. Addition of acetylcholine at 1CH to 10~ g/ml did not affect basal tension, but larger doses (5 X 1CH to 5 X 1CH g/ml) caused a contraction of the strips which varied from slight to marked. Acetylcholine at 1CH to 1CH g/ml caused a further increase in tension when it was added to strips already contracted by norepinephrine, tyramine, KC1, or BaCl2; in contrast, similar doses of acetylcholine caused relaxation of strips contracted by liberation of norepinephrine from the nerve terminals by electrical stimulation (1—10 cps). This relaxation was not influenced by propranolol or hexamethonium but was abolished by atropine (10" g/ml). In intact dogs, the lateral saphenous vein was perfused with autologous blood at constant flow. A sustained venoconstriction was induced either by electrical stimulation of the lumbar sympathetic chain or by a continuous infusion of norepinephrine. An infusion of acetylcholine (10~ to l(h® g/ml min-) relaxed veins constricted by sympathetic stimulation but not those constricted by norepinephrine. Thus, acetylcholine, in doses smaller than those known to have a direct constrictor effect, causes relaxation of cutaneous veins, probably by inhibiting the release of norepinephrine from nerve terminals.