AIM: Dependence of the melatonin-evoked potentiation of the rat tail artery neurogenic reactivity on degree of the change in the reactivity was studied. METHOD: Electrical field stimulation-evoked contractile response of the juvenile rat tail artery segment under isometric conditions was recorded. 0.1 mum melatonin was administered after the change in the response produced both spontaneously and by acidification (pH 6.6) or alkalinization (pH 7.8) of the solution. RESULTS: During the course of experiment, the contraction force continuously declined, being reduced by 12 +/- 5, 24 +/- 7 and 32 +/- 6% at 20, 70, and 170 min after beginning of experiment, respectively. Melatonin applied at these time points increased the contraction by 20 +/- 5, 41 +/- 10, and 48 +/- 8%, respectively, relative to control. This increase in potentiating effect of melatonin during the course of experiment was not because of sensitization of the segment to the hormone. Acidosis-induced considerable decline in neurogenic contraction was counteracted by melatonin, while after alkalosis-induced augmentation in the contraction the hormone was not effective. Melatonin increased the artery response to 0.1 mum noradrenaline. CONCLUSION: These data suggest that melatonin can restore an attenuated neurogenic reactivity of the juvenile rat tail artery. The effect is more pronounced with further decrease in reactivity and might be due to a change in sensitivity of the post-junctional membrane to noradrenaline.
AIM: Dependence of the melatonin-evoked potentiation of the rat tail artery neurogenic reactivity on degree of the change in the reactivity was studied. METHOD: Electrical field stimulation-evoked contractile response of the juvenile rat tail artery segment under isometric conditions was recorded. 0.1 mum melatonin was administered after the change in the response produced both spontaneously and by acidification (pH 6.6) or alkalinization (pH 7.8) of the solution. RESULTS: During the course of experiment, the contraction force continuously declined, being reduced by 12 +/- 5, 24 +/- 7 and 32 +/- 6% at 20, 70, and 170 min after beginning of experiment, respectively. Melatonin applied at these time points increased the contraction by 20 +/- 5, 41 +/- 10, and 48 +/- 8%, respectively, relative to control. This increase in potentiating effect of melatonin during the course of experiment was not because of sensitization of the segment to the hormone. Acidosis-induced considerable decline in neurogenic contraction was counteracted by melatonin, while after alkalosis-induced augmentation in the contraction the hormone was not effective. Melatonin increased the artery response to 0.1 mum noradrenaline. CONCLUSION: These data suggest that melatonin can restore an attenuated neurogenic reactivity of the juvenile rat tail artery. The effect is more pronounced with further decrease in reactivity and might be due to a change in sensitivity of the post-junctional membrane to noradrenaline.