Dietary Potassium Supplementation Reduces Chronic Kidney Lesions Independent of Blood Pressure in Deoxycorticosterone-Acetate and High Sodium Chloride-Treated Mice.

Autor: Wang Q; Division of Nephrology and Hypertension, Lausanne University Hospital (CHUV), 1011 Lausanne, Switzerland., Schäfer SC; Institute for Pathology, Uniklink Köln, Kerpener Strasse 62, 50937 Köln, Germany., Haefliger JA; Department of Biomedical Sciences, Faculty of Biology and Medicine, Lausanne University, Bugnon 7a, 1005 Lausanne, Switzerland., Maillard MP; Division of Nephrology and Hypertension, Lausanne University Hospital (CHUV), 1011 Lausanne, Switzerland., Alonso F; BioTis, Université de Bordeaux, INSERM U1026, 146 Rue Léo Saignat, 33076 Bordeaux, Cedex, France.
Jazyk: angličtina
Zdroj: International journal of molecular sciences [Int J Mol Sci] 2023 Nov 28; Vol. 24 (23). Date of Electronic Publication: 2023 Nov 28.
DOI: 10.3390/ijms242316858
Abstrakt: We have previously shown that an excess of deoxycorticosterone acetate and high sodium chloride intake (DOCA/salt) in one-renin gene mice induces a high urinary Na/K ratio, hypokalemia, and cardiac and renal hypertrophy in the absence of hypertension. Dietary potassium supplementation prevents DOCA/salt-induced pathological processes. In the present study, we further study whether DOCA/salt-treated mice progressively develop chronic inflammation and fibrosis in the kidney and whether dietary potassium supplementation can reduce the DOCA/salt-induced renal pathological process. Results showed that (1) long-term DOCA/salt-treated one-renin gene mice developed severe kidney injuries including tubular/vascular hypertrophy, mesangial/interstitial/perivascular fibrosis, inflammation (lymphocyte's immigration), proteinuria, and high serum creatinine in the absence of hypertension; (2) there were over-expressed mRNAs of plasminogen activator inhibitor-1 (PAI-1), fibronectin, collagen type I and III, interferon-inducible protein-10 (IP-10), monocyte chemotactic protein-1 (MCP1), transforming growth factor- β (TGF- β ), tumor necrosis factor-alpha (TNF- α ), osteopontin, Nuclear factor kappa B (NF-κB)/P65, and intercellular adhesion molecule (ICAM)-1; and (3) dietary potassium supplementation normalized urinary Na/K ratio, hypokalemia, proteinuria, and serum creatinine, reduced renal hypertrophy, inflammations, and fibrosis, and down-regulated mRNA expression of fibronectin, Col-I and III, TGF- β , TNF- α , osteopontin, and ICAM without changes in the blood pressure. The results provide new evidence that potassium and sodium may modulate proinflammatory and fibrotic genes, leading to chronic renal lesions independent of blood pressure.
Databáze: MEDLINE
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