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. 2024 Aug 3;12(8):1751.
doi: 10.3390/biomedicines12081751.

Cardiovascular and Renal Effects Induced by Alpha-Lipoic Acid Treatment in Two-Kidney-One-Clip Hypertensive Rats

Déborah Victória Gomes Nascimento  1 , Darlyson Ferreira Alencar  2 , Matheus Vinicius Barbosa da Silva  1 , Danilo Galvão Rocha  3 , Camila Ferreira Roncari  3 , Roberta Jeane Bezerra Jorge  2   3 , Renata de Sousa Alves  2 , Richard Boarato David  3 , Wylla Tatiana Ferreira E Silva  1 , Lígia Cristina Monteiro Galindo  1 , Thyago Moreira de Queiroz  1
Affiliations

Cardiovascular and Renal Effects Induced by Alpha-Lipoic Acid Treatment in Two-Kidney-One-Clip Hypertensive Rats

Déborah Victória Gomes Nascimento et al. Biomedicines. .

Abstract

α-Lipoic acid (LA) is an antioxidant of endogenous production, also obtained exogenously. Oxidative stress is closely associated with hypertension, which causes kidney injury and endothelial dysfunction. Here, we evaluated the cardiovascular and renal effects of LA in the two-kidney-one-clip (2K1C) hypertension model. The rats were divided into four groups: Sham surgery (Sham), the two-kidneys-one-clip (2K1C) group, and groups treated with LA for 14 days (Sham-LA and 2K1C-LA). No changes were observed in the pattern of food, water intake, and urinary volume. The left/right kidney weight LKw/RKw ratio was significantly higher in 2K1C animals. LA treatment did not reverse the increase in cardiac mass. In relation to vascular reactivity, there was an increase in the potency of phenylephrine (PHE) curve in the hypertensive animals treated with LA compared to the 2K1C group and also compared to the Sham group. Vasorelaxation induced by acetylcholine (Ach) and sodium nitroprusside (SNP) were not improved by treatment with LA. Urea and creatinine levels were not altered by the LA treatment. In conclusion, the morphological changes in the aorta and heart were not reversed; however, the treatment with LA mitigated the contraction increase induced by the 2K1C hypertension.

Keywords: 2K1C; antioxidant; hypertension; lipoic acid; oxidative stress; renal function; renin–angiotensin system; vascular reactivity.

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Conflict of interest statement

The authors declare no conflicts of interest. The funders had no role in the design of the study; in the collection, analyses, or interpretation of data; in the writing of the manuscript; or in the decision to publish the results.

Figures

Figure 1
Figure 1
Effects of LA treatment on water intake and urinary levels. (A) Daily water intake, (B) mean water intake, (C) temporal progression of urinary volume, and (D) urine volume. Data are expressed as mean ± SEM. Comparisons between groups by one-way ANOVA associated with Tukey’s post-test.
Figure 2
Figure 2
Effects of LA treatment on food intake. (A) Temporal progression of food intake and (B) average daily food intake. Data are expressed as mean ± SEM. Comparisons between groups by one-way ANOVA associated with Tukey’s post-test.
Figure 3
Figure 3
Effects of LA treatment on mean arterial pressure during the weeks (A) and the area under the curve graph of the MAP (B). Graph (C) represents the left kidney (LK)/right kidney (RK) ratio. Data expressed as mean ± SEM. Comparisons between groups by one-way ANOVA associated with Tukey’s post-test. * Denotes a significant difference concerning the Sham group (p < 0.05). # Denotes a significant difference in relation to the Sham-LA group (p < 0.05).
Figure 4
Figure 4
Effects of LA treatment on relationship between kidney weight and body weight. (A) Right kidney/body weight ratio and (B) left kidney/body weight ratio. Data expressed as mean ± SEM. Comparisons between groups by one-way ANOVA associated with Tukey’s post-test.
Figure 5
Figure 5
Effects of LA treatment on relationship between heart weight and body weight. Data expressed as mean ± standard deviation. * Denotes a significant difference with the Sham group; # vs. Sham-LA group (p < 0.05). Data expressed as mean ± SEM. Comparisons between groups by one-way ANOVA associated with Tukey’s post-test.
Figure 6
Figure 6
Effects of alpha lipoic acid treatment on endothelium-dependent and -independent relaxation and contractile response to phenylephrine in 2K1C rats. Concentration–response curves for increasing concentrations of (A) acetylcholine (ACh), (B) phenylephrine (PHE), and (C) sodium nitroprusside (SNP). Values are expressed as mean ± SEM. Comparisons between groups by one-way ANOVA associated with Tukey’s post-test.
Figure 7
Figure 7
Analysis of renal function according to urinary creatinine and urea clearance. Creatinine concentration (A) and urea concentration (B). Comparisons between groups by one-way ANOVA associated with Tukey’s post-test (2K1C-LA vs. 2K1C group, p = 0.3116; 2K1C-LA vs. Sham group, p = 0.0771).
Figure 8
Figure 8
Histomorphometric analysis of the heart and aorta. (A) Aortic lumen area, (B) tunica adventitia/media ratio, (C) cardiomyocyte area, (D) cardiomyocyte volume. Comparisons between groups by one-way ANOVA associated with Tukey’s post-test.
Figure 9
Figure 9
Histological analysis of abdominal aorta ring determined by HE. (A) Sham, (B) Sham-LA, (C) 2K1C, and (D) 2K1C-LA. Scale bar  =  500 μm, 100×.
Figure 10
Figure 10
Histological analysis of heart determined by HE. (A) Sham, (B) Sham-LA, (C) 2K1C, and (D) 2K1C-LA. Scale bar =  50 μm, 400×.
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References

    1. James P.A., Oparil S., Carter B.L., Cushman W.C., Dennison-Himmelfarb C., Handler J., Lackland D.T., Lefevre M.L., MacKenzie T.D., Ogedegbe O., et al. 2014 Evidence-Based Guideline for the Management of High Blood Pressure in Adults. JAMA. 2014;311:507. doi: 10.1001/jama.2013.284427. - DOI - PubMed
    1. Herrington W., Lacey B., Sherliker P., Armitage J., Lewington S. Epidemiology of Atherosclerosis and the Potential to Reduce the Global Burden of Atherothrombotic Disease. Circ. Res. 2016;118:535–546. doi: 10.1161/CIRCRESAHA.115.307611. - DOI - PubMed
    1. Patrick D.M., Van Beusecum J.P., Kirabo A. The role of inflammation in hypertension: Novel concepts. Curr. Opin. Physiol. 2021;19:92–98. doi: 10.1016/j.cophys.2020.09.016. - DOI - PMC - PubMed
    1. Mannemuddhu S.S., Ojeda J.C., Yadav A. Renovascular Hypertension. Prim. Care Clin. Off. Pr. 2020;47:631–644. doi: 10.1016/j.pop.2020.08.009. - DOI - PubMed
    1. Iversen B.M., Heyeraas K.J., Sekse I., Andersen K.J., Ofstad J. Autoregulation of renal blood flow in two-kidney, one-clip hypertensive rats. Am. J. Physiol. Physiol. 1986;251:F245–F250. doi: 10.1152/ajprenal.1986.251.2.F245. - DOI - PubMed

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