Abstract
Renal and cardiac impairments are frequent events in the presence of hypertension. Organ damage is mainly linked to oxidative stress due to high blood pressure and may be reduced by antioxidant supplementation. Alpha-lipoic acid (ALA) is one of most effective antioxidants. It is widely used as a nutritional supplement in a racemic mixture (+/–), even though the (+)-enantiomer is biologically active. This study was designed to investigate the effect of treatment with (+/–)-ALA and its enantiomers on renal and heart parenchyma in spontaneously hypertensive rats (SHR), using immunochemical and immunohistochemical techniques. The results confirmed that the oxidative mechanisms of organ alterations, due to hypertension, and characterized by glomerular and tubular lesions, left ventricular hypertrophy, and fibrosis but not by apoptosis were accompanied by proteins’ and nucleic acids’ oxidation. We found greater effectiveness of (+)-ALA compared to (+/−)-ALA in reducing oxidative stress, cardiac and renal damages in SHR. To conclude, these data propose (+)-ALA as one of the more appropriate antioxidant molecules to prevent renal and cardiac alterations associated with hypertension.
Highlights
Hypertension is a multifactorial disease characterized by elevated blood pressure.It is a risk factor for renal and cardiovascular diseases [1,2]
The systolic blood pressure values were higher in control spontaneously hypertensive rats (SHR) rats (215 ± 3 mmHg) compared to the normotensive Wistar–Kyoto rats (WKY) rats
Arterial hypertension can can be generated by numerous factors, suchsuch as lifestyle, physioArterial hypertension be generated by numerous factors, as lifestyle, physlogical and genetic causes
Summary
Hypertension is a multifactorial disease characterized by elevated blood pressure. It is a risk factor for renal and cardiovascular diseases [1,2]. Both the kidney and the heart are target organs in hypertension, and their structure and function become gradually impaired with longstanding hypertension. Multiple mechanisms are implicated in the determination of hypertension-induced kidney damage. These involve different cell types and anatomical structures in the kidney, including the glomeruli, tubulointerstitium, immune cells, and vasculature. Other histopathological alterations are interstitial fibrosis, associated with tubular atrophy, and arteriosclerosis of the afferent arterioles [1,5]
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