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In recent years, experimental evidence have been suggested that melatonin has either contractive or relaxing effects on the vascular smooth muscle in vitro. but the effect of melatonin on the cardiovascular system in vivo had been emphasized about the hypotensive effect. In this work, we found not only hypotensive effct but also hypertensive effct of melatonin in rats and attempted to determine the mechanism of these effects elicited by melatonin. Regadless of concentration, melatonin(0.002~5mg/kg) produced increase in mean blood pressure (MBP) in 36% (54/150 cases) and decrease in mean blood pressure in 64%(96/150cases). As a whole melatonin caused and increase or d decrease in MBP without compensatory decrease or increase in heart rate. The mlatonin-induced hypertension was abolished by the pretreatment of phenoxybenzamine, a α-adrenoceptor antagoninst. The melatonin-induced hypotension was abolished by the pretreatment of propranolol, a β-adrenoceptor antagonist, ODQ, a NO-sensitive guanylate cyclase inhibitor, or nifedipine, a L-type Ca^2+ channel blocker, but not by bilateral cervical vagotomy. The results indicate that melatonin-induced hypertension may be related to α-adrenoceptor stimulation and melatonin-indued hypotension may be related to β-adrenoceptor stimulation, inhibition of Ca^2+ channel and/or activation of guanylate cyclase.
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