The vascular reactivity of melatonin

1. Melatonin receptors have been located in the vasculature. The present study investigates the hypothesis that melatonin can alter vascular contraction. 2. Helical strips of endothelium-intact rat thoracic aorta and endothelium-denuded mesenteric and endothelium-denuded caudal arteries were mounted in isolated tissue baths for measurement of isometric contractile force. Melatonin (10(-12)-10(-3) M) did not cause contraction in the thoracic aorta, the mesenteric artery or the caudal artery. In the same arteries contracted with phenylephrine, melatonin (10(-12)-10(-3) M) did not cause direct relaxation. 3. In the rat aorta, a test for inhibition of KCl-induced contraction was conducted. Melatonin (10(-5)-10(-3) M) and the melatonergic agonist N-acetylserotonin (10(-5) M) inhibited contraction to KCl. The percentage inhibition observed at 70 mM KCl were as follows for melatonin: [25.3% (1 x 10(-5) M), 32.0% (1 x 10(-4) M), 26.4% (3 x 10(-4) M), 52.4% (1 x 10(-3) M); N-acetylserotonin 26.7% (1 x 10(-5) M), no inhibition at (1 x 10(-3) M)]. The melatonergic antagonist luzindole (2 x 10(-6) M) did not inhibit the melatonin (10(-3) M)-induced inhibition of KCl contraction in the rat aorta. 4. The possible effect that melatonin may have on endothelial nitric oxide activity also was examined. Melatonin (10(-5) M) did not affect acetylcholine (10(-9)-10(-4) M)-induced relaxation in the rat aorta contracted with a half-maximal concentration of phenylephrine. 5. These data suggest that melatonin can inhibit rat vascular reactivity but does so largely in a non-specific manner.