ArticleOxidative medicine and cellular longevity2022
Vascular Endothelial Dysfunction in the Thoracic Aorta of Rats with Ischemic Acute Kidney Injury: Contribution of Indoxyl Sulfate.
Article in Oxidative medicine and cellular longevity, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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6 citing papers in PubMed, 8 citations in OpenAlex.
- Delayed conception or sildenafil prevents endothelial dysfunction in pregnant rats after renal ischemia-reperfusion.American journal of physiology. Renal physiology · 2026Article
- Renal Ischemia-Reperfusion and Uremic Toxins Modulate the Aortic Adenosinergic Axis in Acute Kidney Injury.International journal of molecular sciences · 2026Article
- AST-120 alleviates renal ischemia-reperfusion injury by inhibiting HK2-mediated glycolysis.Molecular medicine (Cambridge, Mass.) · 2024Article
- Indoxyl Sulfate Administration during Pregnancy Contributes to Renal Injury and Increased Blood-Brain Barrier Permeability.International journal of molecular sciences · 2023Article
- Review
- Microbiota-derived tryptophan metabolites in vascular inflammation and cardiovascular disease.Amino acids · 2022Review
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9 authors at 2 institutions in 1 country.
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Abstract
Chronic kidney disease (CKD) and cardiovascular disease are known to be linked, and the involvement of indoxyl sulfate (IS), a type of uremic toxin, has been suggested as one of the causes. It is known that IS induces vascular dysfunction through overproduction of reactive oxygen species (ROS). On the other hand, the involvement of IS in the vascular dysfunction associated with acute kidney injury (AKI) is not fully understood. Therefore, we investigated this issue using the thoracic aorta of rats with ischemic AKI. Ischemic AKI was induced by occlusion of the left renal artery and vein for 45 min, followed by reperfusion 2 weeks after contralateral nephrectomy. One day after reperfusion, there was marked deterioration in renal function evidenced by an increase in plasma creatinine. Furthermore, blood IS levels increased markedly due to worsening renal function. Seven days and 28 days after reperfusion, blood IS levels decreased with the improvement in renal function. Of note, acetylcholine-induced vasorelaxation deteriorated over time after reperfusion, contradicting the recovery of renal function. In addition, 28 days after reperfusion, we observed a significant increase in ROS production in the vascular tissue. Next, we administered AST-120, a spherical adsorbent charcoal, after reperfusion to assess whether the vascular endothelial dysfunction associated with the ischemic AKI was due to a temporary increase in blood IS levels. AST-120 reduced the temporary increase in blood IS levels after reperfusion without influencing renal function, but did not restore the impaired vascular reactivity. Thus, in ischemic AKI, we confirmed that the vascular endothelial function of the thoracic aorta is impaired even after the recovery of kidney injury, probably with excessive ROS production. IS, which increases from ischemia to early after reperfusion, may not be a major contributor to the vascular dysfunction associated with ischemic AKI.
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