期刊
JOURNAL OF PINEAL RESEARCH
卷 65, 期 4, 页码 -出版社
WILEY
DOI: 10.1111/jpi.12513
关键词
arrhythmias; chronic kidney disease; cytoprotective effects; melatonin; obstructive nephropathy; oxidative stress; reperfusion injury
资金
- Secretaria de Ciencia, Tecnica y Postgrado, Universidad Nacional de Cuyo
- ANPCyT (Agencia Nacional de Promocion de la Ciencia y la Tecnologia) [PICT 2012-0234]
Lethal ventricular arrhythmias increase in patients with chronic kidney disease that suffer an acute coronary event. Chronic kidney disease induces myocardial remodeling, oxidative stress, and arrhythmogenesis. A manifestation of the relationship between kidney and heart is the concomitant reduction in vitamin D receptor (VDR) and the increase in angiotensin II receptor type 1 (AT(1)). Melatonin has renal and cardiac protective actions. One potential mechanism is the increase in the heat shock protein 70 (Hsp70)-an antioxidant factor. We aim to determine the mechanisms involved in melatonin (Mel) prevention of kidney damage and arrhythmogenic heart remodeling. Unilateral ureteral-obstruction (UUO) and sham-operated rats were treated with either melatonin (4 mg/kg/day) or vehicle for 15 days. Hearts and kidneys from obstructed rats showed a reduction in VDR and Hsp70. Associated with AT(1) up-regulation in the kidneys and the heart of UUO rats also increased oxidative stress, fibrosis, apoptosis, mitochondrial edema, and dilated crests. Melatonin prevented these changes and ventricular fibrillation during reperfusion. The action potential lengthened and hyperpolarized in melatonin-treated rats throughout the experiment. We conclude that melatonin prevents renal damage and arrhythmogenic myocardial remodeling during unilateral ureteral obstruction due to a decrease in oxidative stress/fibrosis/apoptosis associated with AT(1) reduction and Hsp70-VDR increase.
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