Abstract
The role of the renin-angiotensin system (RAS) in blood pressure regulation in MS during aging is unknown. It participates in metabolic syndrome (MS) and aging regulating vascular tone and remodeling. RAS might participate in a compensatory mechanism decreasing blood pressure and allowing MS rats to reach 18 months of age and it might form part of therapeutical procedures to ameliorate MS. We studied histological changes and distribution of RAS receptors in aortas of MS aged rats. Electron microscopy images showed premature aging in MS since the increased fibrosis, enlarged endothelium, and invasion of this layer by muscle cells that was present in control 18-month-old aortas were also found in 6-month-old aortas from MS rats. AT1, AT2, and Mas receptors mediate the effects of Ang II and Ang 1-7, respectively. Fluorescence from AT2 decreased with age in control and MS aortas, while fluorescence of AT1 increased in aortas from MS rats at 6 months and diminished during aging. Mas expression increased in MS rats and remained unchanged in control rats. In conclusion, there is premature aging in the aortas from MS rats and the elevated expression of Mas receptor might contribute to decrease blood pressure during aging in MS.
Highlights
Metabolic syndrome (MS) is a disease that accelerates aging [1]
Fasting serum glucose levels were not significantly different among the groups, but there was an increase at 18 months in MS rats
Blood pressure is controlled by baroreflex activity that modulates sympathetic neural mechanisms and by central nervous set points that adjust its long-term level
Summary
Aging is associated with endothelial dysfunction and structural and functional vascular changes [2]. Rats that survive to reach 18 months are few and could be the ones that develop compensatory mechanisms to the effects of MS, the fall of arterial pressure being one of them [3, 4]. These compensatory mechanisms might be the same that underlie the condition of healthy obese or healthy MS patients and could be the basis for the development of therapeutical approaches to complications of MS. The renin angiotensin system (RAS) might participate in these mechanisms and the Ang 1-7/MAS pathway
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