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Effect of angiotensin-converting enzyme blockade, alone or combined with blockade of soluble epoxide hydrolase, on the course of congestive heart failure and occurrence of renal dysfunction in Ren-2 transgenic hypertensive rats with aorto-caval fistula

P. Kala, L. Sedláková, P. Škaroupková, L. Kopkan, Z. Vaňourková, M. Táborský, A. Nishiyama, S. H. Hwang, B. D. Hammock, J. Sadowski, V. Melenovský, J. D. Imig, L. Červenka

. 2018 ; 67 (3) : 401-415. [pub] 20180312

Language English Country Czech Republic

Document type Journal Article

Persistent link   https://www.medvik.cz/link/bmc18040228

We showed recently that increasing kidney epoxyeicosatrienoic acids (EETs) by blocking soluble epoxide hydrolase (sEH), an enzyme responsible for EETs degradation, retarded the development of renal dysfunction and progression of aorto-caval fistula(ACF)-induced congestive heart failure (CHF) in Ren-2 transgenic hypertensive rats (TGR). In that study the final survival rate of untreated ACF TGR was only 14 % but increased to 41 % after sEH blockade. Here we examined if sEH inhibition added to renin-angiotensin system (RAS) blockade would further enhance protection against ACF-induced CHF in TGR. The treatment regimens were started one week after ACF creation and the follow-up period was 50 weeks. RAS was blocked using angiotensin-converting enzyme inhibitor (ACEi, trandolapril, 6 mg/l) and sEH with an sEH inhibitor (sEHi, c-AUCB, 3 mg/l). Renal hemodynamics and excretory function were determined two weeks post-ACF, just before the onset of decompensated phase of CHF. 29 weeks post-ACF no untreated animal survived. ACEi treatment greatly improved the survival rate, to 84 % at the end of study. Surprisingly, combined treatment with ACEi and sEHi worsened the rate (53 %). Untreated ACF TGR exhibited marked impairment of renal function and the treatment with ACEi alone or combined with sEH inhibition did not prevent it. In conclusion, addition of sEHi to ACEi treatment does not provide better protection against CHF progression and does not increase the survival rate in ACF TGR: indeed, the rate decreases significantly. Thus, combined treatment with sEHi and ACEi is not a promising approach to further attenuate renal dysfunction and retard progression of CHF.

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$a We showed recently that increasing kidney epoxyeicosatrienoic acids (EETs) by blocking soluble epoxide hydrolase (sEH), an enzyme responsible for EETs degradation, retarded the development of renal dysfunction and progression of aorto-caval fistula(ACF)-induced congestive heart failure (CHF) in Ren-2 transgenic hypertensive rats (TGR). In that study the final survival rate of untreated ACF TGR was only 14 % but increased to 41 % after sEH blockade. Here we examined if sEH inhibition added to renin-angiotensin system (RAS) blockade would further enhance protection against ACF-induced CHF in TGR. The treatment regimens were started one week after ACF creation and the follow-up period was 50 weeks. RAS was blocked using angiotensin-converting enzyme inhibitor (ACEi, trandolapril, 6 mg/l) and sEH with an sEH inhibitor (sEHi, c-AUCB, 3 mg/l). Renal hemodynamics and excretory function were determined two weeks post-ACF, just before the onset of decompensated phase of CHF. 29 weeks post-ACF no untreated animal survived. ACEi treatment greatly improved the survival rate, to 84 % at the end of study. Surprisingly, combined treatment with ACEi and sEHi worsened the rate (53 %). Untreated ACF TGR exhibited marked impairment of renal function and the treatment with ACEi alone or combined with sEH inhibition did not prevent it. In conclusion, addition of sEHi to ACEi treatment does not provide better protection against CHF progression and does not increase the survival rate in ACF TGR: indeed, the rate decreases significantly. Thus, combined treatment with sEHi and ACEi is not a promising approach to further attenuate renal dysfunction and retard progression of CHF.
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$a Sedláková, Lenka, $d 1992- $7 xx0273377 $u Center for Experimental Medicine, Institute for Clinical and Experimental Medicine, Prague, Czech Republic
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$a Škaroupková, Petra $7 xx0117683 $u Center for Experimental Medicine, Institute for Clinical and Experimental Medicine, Prague, Czech Republic
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$a Kopkan, Libor $7 xx0107287 $u Center for Experimental Medicine, Institute for Clinical and Experimental Medicine, Prague, Czech Republic
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$a Táborský, Miloš, $d 1962- $7 jn20010310074 $u Department of Internal Medicine I, Cardiology, University Hospital Olomouc and Palacký University, Olomouc Czech Republic
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$a Nishiyama, A. $u Department of Pharmacology, Kagawa University, Kagawa, Japan
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$a Hwang, S. H. $u Department of Entomology and UCD Cancer Center, University of California, Davis, CA, USA
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$a Hammock, B. D. $u Department of Entomology and UCD Cancer Center, University of California, Davis, CA, USA
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$a Sadowski, J. $u Department of Renal and Body Fluid Physiology, Mossakowski Medical Research Centre, Polish Academy of Science, Warsaw, Poland
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$a Melenovský, Vojtěch $7 xx0160847 $u Department of Cardiology, Institute for Clinical and Experimental Medicine, Prague, Czech Republic
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$a Imig, J. D. $u Department of Pharmacology and Toxicology, Medical College of Wisconsin, Milwaukee, WI, USA
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$a Červenka, Luděk, $d 1967- $7 xx0037105 $u Center for Experimental Medicine, Institute for Clinical and Experimental Medicine, Prague, Czech Republic; Department of Pathophysiology, Second Faculty of Medicine, Charles University, Prague, Czech Republic
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