Melatonin potentiates NE-induced vasoconstriction without augmenting cytosolic calcium concentration

Because little is known of the intracellular mechanisms involved in the vas oconstrictor effect of melatonin (Mel), we examined the in vitro effects of Mel by using perfused cylindrical segments of the rat tail artery loaded w ith the intracellular Ca2+ concentration ([Ca2+](i))-sensitive fluorescent dye, fura 2. Mel (10(-14) to 10(-4) M) had no effect on baseline perfusion pressure or [Ca2+](i) but increased, at submicromolar concentrations, the v asoconstrictor effect of norepinephrine (NE) (P = 0.0029). Mel did not modi fy NE-induced [Ca2+](i) mobilization, and thus the [Ca2+](i) sensitivity of NE-induced contraction increased in the presence of Mel. Mel consistently increased KCl-induced vasoconstriction and [Ca2+](i) sensitivity of contrac tion, but differences were not statistically significant. In conclusion, Me l increases the [Ca2+](i) sensitivity of vasoconstriction evoked by NE sugg esting that Mel may amplify endogenous vasoconstrictor responses to sympath etic outflow.