ABSTRACT
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.
