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DOI 10.1038/ajh.2007.60

Медицинская библиотека · American journal of hypertension · 2008

The role of melatonin in the pathogenesis of hypertension in rats with metabolic syndrome.

Leibowitz Avshalom, Peleg Edna, Sharabi Yhenoatan, Shabtai Zehava, Shamiss Ari, Grossman Ehud

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Аннотация

BACKGROUND

Melatonin, the primary hormone of the pineal gland, is a known modulator of various physiological processes. The aim of this study was to evaluate the role of melatonin in the pathogenesis of hypertension in rats with metabolic syndrome and to assess whether melatonin supplementation prevents the development of hypertension in this model.

METHODS

Twenty male Sprague-Dawley (SD) rats were fed either a high fructose diet (n = 10) or a regular diet (control; n = 10) for 5 weeks. Urinary excretion of 6-hydroxymelatoninsulfate (a metabolite of melatonin) was measured at the beginning and the end of the study. An additional 20 SD rats were fed with the same diets but with a supplementation of melatonin (30 mg/kg/day) in their drinking water. Blood pressure (BP) was measured every week.

RESULTS

BP increased significantly in rats fed with a high fructose diet and remained unchanged in the control group. The BP rise was associated with a significant decrease in melatonin secretion during sleep. Melatonin supplementation prevented the BP rise in fructose fed rats. BP increased by 14.6 +/- 1.0 mm Hg in the fructose fed rats, whereas it increased by only 3 +/- 2.6 mm Hg in rats fed with fructose and melatonin (P < 0.001 between groups).

CONCLUSIONS

Melatonin secretion decreased in fructose fed rats that developed hypertension. Administration of melatonin blunted this BP rise. These data suggested that melatonin plays a role in the pathogenesis of hypertension in rats with metabolic syndrome.

Для цитирования: Leibowitz Avshalom, Peleg Edna, Sharabi Yhenoatan, Shabtai Zehava, Shamiss Ari, Grossman Ehud. The role of melatonin in the pathogenesis of hypertension in rats with metabolic syndrome.. American journal of hypertension. 2008. DOI: 10.1038/ajh.2007.60.

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