Endothelin type A receptor blockade attenuates aorto-caval fistula-induced heart failure in rats with angiotensin II-dependent hypertension

Kód výsledku v IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F67985823%3A_____%2F23%3A00570226" target="_blank" >RIV/67985823:_____/23:00570226 - isvavai.cz</a>

Nalezeny alternativní kódy

RIV/00023001:_____/23:00083716 RIV/00216208:11130/23:10448594 RIV/61989592:15110/23:73618651 RIV/00098892:_____/23:10157833 RIV/00064203:_____/23:10448594

Výsledek na webu

<a href="https://journals.lww.com/jhypertension/Fulltext/2023/01000/Endothelin_type_A_receptor_blockade_attenuates.11.aspx" target="_blank" >https://journals.lww.com/jhypertension/Fulltext/2023/01000/Endothelin_type_A_receptor_blockade_attenuates.11.aspx</a>

DOI - Digital Object Identifier

<a href="http://dx.doi.org/10.1097/HJH.0000000000003307" target="_blank" >10.1097/HJH.0000000000003307</a>

Jazyk výsledku

angličtina

Název v původním jazyce

Endothelin type A receptor blockade attenuates aorto-caval fistula-induced heart failure in rats with angiotensin II-dependent hypertension

Popis výsledku v původním jazyce

Objective:Evaluation of the effect of endothelin type A (ETA) receptor blockade on the course of volume-overload heart failure in rats with angiotensin II-dependent hypertension.Methods:Ren-2 renin transgenic rats (TGR) were used as a model of hypertension. Heart failure was induced by creating an aorto-caval fistula (ACF). Selective ETA receptor blockade was achieved by atrasentan. For comparison, other rat groups received trandolapril, an angiotensin-converting enzyme inhibitor (ACEi). Animals first underwent ACF creation and 2 weeks later the treatment with atrasentan or trandolapril, alone or combined, was applied, the follow-up period was 20 weeks.Results:Eighteen days after creating ACF, untreated TGR began to die, and none was alive by day 79. Both atrasentan and trandolapril treatment improved the survival rate, ultimately to 56% (18 of 31 animals) and 69% (22 of 32 animals), respectively. Combined ACEi and ETA receptor blockade improved the final survival rate to 52% (17 of 33 animals). The effects of the three treatment regimens on the survival rate did not significantly differ. All three treatment regimens suppressed the development of cardiac hypertrophy and lung congestion, decreased left ventricle (LV) end-diastolic volume and LV end-diastolic pressure, and improved LV systolic contractility in ACF TGR as compared with their untreated counterparts.Conclusion:The treatment with ETA receptor antagonist delays the onset of decompensation of volume-overload heart failure and improves the survival rate in hypertensive TGR with ACF-induced heart failure. However, the addition of ETA receptor blockade did not enhance the beneficial effects beyond those obtained with standard treatment with ACEi alone.

Název v anglickém jazyce

Endothelin type A receptor blockade attenuates aorto-caval fistula-induced heart failure in rats with angiotensin II-dependent hypertension

Popis výsledku anglicky

Objective:Evaluation of the effect of endothelin type A (ETA) receptor blockade on the course of volume-overload heart failure in rats with angiotensin II-dependent hypertension.Methods:Ren-2 renin transgenic rats (TGR) were used as a model of hypertension. Heart failure was induced by creating an aorto-caval fistula (ACF). Selective ETA receptor blockade was achieved by atrasentan. For comparison, other rat groups received trandolapril, an angiotensin-converting enzyme inhibitor (ACEi). Animals first underwent ACF creation and 2 weeks later the treatment with atrasentan or trandolapril, alone or combined, was applied, the follow-up period was 20 weeks.Results:Eighteen days after creating ACF, untreated TGR began to die, and none was alive by day 79. Both atrasentan and trandolapril treatment improved the survival rate, ultimately to 56% (18 of 31 animals) and 69% (22 of 32 animals), respectively. Combined ACEi and ETA receptor blockade improved the final survival rate to 52% (17 of 33 animals). The effects of the three treatment regimens on the survival rate did not significantly differ. All three treatment regimens suppressed the development of cardiac hypertrophy and lung congestion, decreased left ventricle (LV) end-diastolic volume and LV end-diastolic pressure, and improved LV systolic contractility in ACF TGR as compared with their untreated counterparts.Conclusion:The treatment with ETA receptor antagonist delays the onset of decompensation of volume-overload heart failure and improves the survival rate in hypertensive TGR with ACF-induced heart failure. However, the addition of ETA receptor blockade did not enhance the beneficial effects beyond those obtained with standard treatment with ACEi alone.

Druh

J_imp - Článek v periodiku v databázi Web of Science

CEP obor

—

OECD FORD obor

30201 - Cardiac and Cardiovascular systems

Projekt

Výsledek vznikl pri realizaci vícero projektů. Více informací v záložce Projekty.

Návaznosti

I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace

Rok uplatnění

2023

Kód důvěrnosti údajů

S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Název periodika

Journal of Hypertension

ISSN

0263-6352

e-ISSN

1473-5598

Svazek periodika

41

Číslo periodika v rámci svazku

1

Stát vydavatele periodika

GB - Spojené království Velké Británie a Severního Irska

Počet stran výsledku

16

Strana od-do

99-114

Kód UT WoS článku

000921029000013

EID výsledku v databázi Scopus

2-s2.0-85143180046