Key result
Doxorubicin-induced HF upregulates renin-angiotensin mRNA in all rats but activates endothelin only in normotensive rats.
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.
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Jíchová et al. (2021) studied Chemotherapy-induced heart failure. Doxorubicin vs. Normotensive (HanSD) vs Ren-2 transgenic hypertensive (TGR) rats was evaluated on mRNA expression of genes implicated in HF-associated cardiorenal syndrome. In doxorubicin-induced heart failure, both normotensive and hypertensive rats showed upregulated renin-angiotensin system mRNA, but endothelin system activation was limited to normotensive rats.
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