Kidney Response to Chemotherapy-Induced Heart Failure: mRNA Analysis in Normotensive and Ren-2 Transgenic Hypertensive Rats

International Journal of Molecular Sciences

Luděk Červenka¹  Petr Kala¹  Šárka Jíchová¹  Lenka Hošková²  Vojtěch Melenovský²  Josef Veselka³  Věra Čertíková Chábová⁴  Olga Gawryś⁵  Janusz Sadowski⁵  Elżbieta Kompanowska-Jezierska⁵ 

[1] Center for Experimental Medicine, Institute for Clinical and Experimental Medicine, 14021 Prague, Czech Republic;Department of Cardiology, Institute for Clinical and Experimental Medicine, 14021 Prague, Czech Republic;Department of Cardiology, University Hospital Motol and 2nd Faculty of Medicine, Charles University, 15006 Prague, Czech Republic;Department of Nephrology, 1st Faculty of Medicine, Charles University, 12108 Prague, Czech Republic;Department of Renal and Body Fluid Physiology, Mossakowski Medical Research Institute, Polish Academy of Sciences, PL02-106 Warsaw, Poland;

关键词: chemotherapy-induced heart failure;    doxorubicin;    hypertension;    kidney;    renin-angiotensin-aldosterone system;    endothelin system;   

DOI  :  10.3390/ijms22168475

来源: DOAJ

【 摘 要 】

The aim of the present study was to perform kidney messenger ribonucleic acid (mRNA) analysis in normotensive, Hannover Sprague–Dawley (HanSD) rats and hypertensive, Ren-2 renin transgenic rats (TGR) after doxorubicin-induced heart failure (HF) with specific focus on genes that are implicated in the pathophysiology of HF-associated cardiorenal syndrome. We found that in both strains renin and angiotensin-converting enzyme mRNA expressions were upregulated indicating that the vasoconstrictor axis of the renin–angiotensin system was activated. We found that pre-proendothelin-1, endothelin-converting enzyme type 1 and endothelin type A receptor mRNA expressions were upregulated in HanSD rats, but not in TGR, suggesting the activation of endothelin system in HanSD rats, but not in TGR. We found that mRNA expression of cytochrome P-450 subfamily 2C23 was downregulated in TGR and not in HanSD rats, suggesting the deficiency in the intrarenal cytochrome P450-dependent pathway of arachidonic acid metabolism in TGR. These results should be the basis for future studies evaluating the pathophysiology of cardiorenal syndrome secondary to chemotherapy-induced HF in order to potentially develop new therapeutic approaches.

【 授权许可】

Unknown