OBJECTIVE: To determine whether the evening intake of 5 mg melatonin affects 24 h arterial blood pressure and heart-rate profiles. METHODS:Twenty-one young normotensive subjects were administered placebo or melatonin for 4 weeks, according to a cross-over double-blind design, and were subjected to ambulatory blood pressure monitoring on the first and last days of each treatment period. RESULTS: The chronic melatonin intake caused a decrease in systolic blood pressure throughout the 24 h period (109.1+/- 7.2 versus 113.6 +/- 8.15 mmHg, P < 0.05), a decrease in diastolic blood pressure (by 6.4 mmHg, P < 0.05) limited to the second half of the night, a slight lowering of the heart rate during the diurnal hours (78.6 +/- 7.6 versus 81.5 +/- 10.1 beats/min, P < 0.05) and an acceleration of a similar degree during the second half of the night. The slight hypotensive action and the diurnal heart-rate lowering may be explained theoretically in terms of various complex and synergistic mechanisms that so far have been verified only in experimental studies on animals. The etiology of the nocturnal heart-rate acceleration remains unknoiwn. Further controlled studies are needed in order to better understand the cardiovascular effects of melatonin and to evaluate possible pharmacologic interactions. CONCLUSION:
RCT Entities:
OBJECTIVE: To determine whether the evening intake of 5 mg melatonin affects 24 h arterial blood pressure and heart-rate profiles. METHODS: Twenty-one young normotensive subjects were administered placebo or melatonin for 4 weeks, according to a cross-over double-blind design, and were subjected to ambulatory blood pressure monitoring on the first and last days of each treatment period. RESULTS: The chronic melatonin intake caused a decrease in systolic blood pressure throughout the 24 h period (109.1+/- 7.2 versus 113.6 +/- 8.15 mmHg, P < 0.05), a decrease in diastolic blood pressure (by 6.4 mmHg, P < 0.05) limited to the second half of the night, a slight lowering of the heart rate during the diurnal hours (78.6 +/- 7.6 versus 81.5 +/- 10.1 beats/min, P < 0.05) and an acceleration of a similar degree during the second half of the night. The slight hypotensive action and the diurnal heart-rate lowering may be explained theoretically in terms of various complex and synergistic mechanisms that so far have been verified only in experimental studies on animals. The etiology of the nocturnal heart-rate acceleration remains unknoiwn. Further controlled studies are needed in order to better understand the cardiovascular effects of melatonin and to evaluate possible pharmacologic interactions. CONCLUSION:
Authors: Abhinav Goyal; Paul D Terry; Hillary M Superak; Christine L Nell-Dybdahl; Ritam Chowdhury; Lawrence S Phillips; Michael H Kutner Journal: Diabetol Metab Syndr Date: 2014-11-18 Impact factor: 3.320