Inhibition by Acetylcholine of Adrenergic Neurotransmission in Vascular Smooth Muscle
Changes in the isometric tension of isolated strips of cutaneous, femoral, mesenteric, pulmonary, and muscle arteries and veins were recorded at 37°C in an organ bath. Acetylcholine (5 x 10-8 and 10-7g/ml) caused relaxation of strips from the saphenous veins, the femoral veins, and all of the arteries after contraction by norepinephrine released from nerve terminals by electrical stimulation (2-5 Hz); in the pulmonary and mesenteric veins, acetylcholine caused a further increase in tension. Pulmonary artery and mesenteric vein strips were incubated with [3H] norepinephrine and mounted for superfusion (3 ml/min) and isometric tension recording. Electrical stimulation increased the tension and the total radioactivity released in both preparations. Acetylcholine (2 x 10-7 g/ml) depressed the contractions of the pulmonary artery strips but augmented those of the mesenteric vein strips; it diminished the efflux of radioactivity in both, indicating that acetylcholine inhibits adrenergic neurotransmission. In the absence of sympathetic stimulation, acetylcholine (5 x 10-10-10-5 g/ml) caused all vein strips to contract; the most common reaction in artery strips was a slight relaxation (at 10-9-10-8g/ml) followed by a contraction (at 5 x 10-8-10-5 g/ml). During contractions caused by norepinephrine, acetylcholine caused a further increase in tension in vein strips but a relaxation in artery strips. Atropine abolished the effects of acetylcholine. The results of this study suggest the presence in vascular smooth muscle of both excitatory and inhibitory cholinergic receptors.
- cholinergic dilation
- isolated veins and arteries
- norepinephrine release
- sympathetic nerve endings
- Received May 29, 1973.
- Accepted December 20, 1973.
- © 1974 American Heart Association, Inc.