-
Je něco špatně v tomto záznamu ?
Endothelin type A receptor blockade attenuates aorto-caval fistula-induced heart failure in rats with angiotensin II-dependent hypertension
P. Kala, O. Gawrys, M. Miklovič, Z. Vaňourková, P. Škaroupková, Š. Jíchová, J. Sadowski, E. Kompanowska-Jezierska, A. Walkowska, J. Veselka, M. Táborský, H. Maxová, I. Vaněčková, L. Červenka
Jazyk angličtina Země Anglie, Velká Británie
Typ dokumentu časopisecké články
- MeSH
- angiotensin II MeSH
- atrasentan MeSH
- endotelin-1 MeSH
- endoteliny MeSH
- hypertenze * komplikace farmakoterapie MeSH
- inhibitory ACE farmakologie MeSH
- krysa rodu rattus MeSH
- píštěle * MeSH
- potkani transgenní MeSH
- receptor angiotensinu typ 1 MeSH
- receptor endotelinu A MeSH
- srdeční selhání * farmakoterapie etiologie MeSH
- zvířata MeSH
- Check Tag
- krysa rodu rattus MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
OBJECTIVE: Evaluation of the effect of endothelin type A (ET A ) 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 ET A 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 ET A 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 ET A 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 ET A receptor blockade did not enhance the beneficial effects beyond those obtained with standard treatment with ACEi alone.
Center for Experimental Medicine Institute for Clinical and Experimental Medicine
Department of Pathophysiology 2nd Faculty of Medicine Charles University
Institute of Physiology of the Czech Academy of Sciences Prague Czech Republic
Citace poskytuje Crossref.org
- 000
- 00000naa a2200000 a 4500
- 001
- bmc22032067
- 003
- CZ-PrNML
- 005
- 20230131150942.0
- 007
- ta
- 008
- 230120s2023 enk f 000 0|eng||
- 009
- AR
- 024 7_
- $a 10.1097/HJH.0000000000003307 $2 doi
- 035 __
- $a (PubMed)36204993
- 040 __
- $a ABA008 $b cze $d ABA008 $e AACR2
- 041 0_
- $a eng
- 044 __
- $a enk
- 100 1_
- $a Kala, Petr $u Center for Experimental Medicine, Institute for Clinical and Experimental Medicine $u Department of Cardiology, University Hospital Motol and 2nd Faculty of Medicine, Charles University, Prague, Czech Republic
- 245 10
- $a Endothelin type A receptor blockade attenuates aorto-caval fistula-induced heart failure in rats with angiotensin II-dependent hypertension / $c P. Kala, O. Gawrys, M. Miklovič, Z. Vaňourková, P. Škaroupková, Š. Jíchová, J. Sadowski, E. Kompanowska-Jezierska, A. Walkowska, J. Veselka, M. Táborský, H. Maxová, I. Vaněčková, L. Červenka
- 520 9_
- $a OBJECTIVE: Evaluation of the effect of endothelin type A (ET A ) 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 ET A 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 ET A 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 ET A 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 ET A receptor blockade did not enhance the beneficial effects beyond those obtained with standard treatment with ACEi alone.
- 650 _2
- $a krysa rodu Rattus $7 D051381
- 650 _2
- $a zvířata $7 D000818
- 650 _2
- $a angiotensin II $7 D000804
- 650 _2
- $a receptor endotelinu A $7 D044022
- 650 _2
- $a atrasentan $7 D000077868
- 650 12
- $a hypertenze $x komplikace $x farmakoterapie $7 D006973
- 650 _2
- $a inhibitory ACE $x farmakologie $7 D000806
- 650 12
- $a srdeční selhání $x farmakoterapie $x etiologie $7 D006333
- 650 _2
- $a potkani transgenní $7 D055647
- 650 12
- $a píštěle $7 D005402
- 650 _2
- $a endoteliny $7 D016232
- 650 _2
- $a endotelin-1 $7 D019332
- 650 _2
- $a receptor angiotensinu typ 1 $7 D044140
- 655 _2
- $a časopisecké články $7 D016428
- 700 1_
- $a Gawrys, Olga $u Center for Experimental Medicine, Institute for Clinical and Experimental Medicine $u Department of Renal and Body Fluid Physiology, Mossakowski Medical Research Institute, Polish Academy of Science, Warsaw, Poland
- 700 1_
- $a Miklovič, Matúš $u Center for Experimental Medicine, Institute for Clinical and Experimental Medicine
- 700 1_
- $a Vaňourková, Zdenka $u Center for Experimental Medicine, Institute for Clinical and Experimental Medicine
- 700 1_
- $a Škaroupková, Petra $u Center for Experimental Medicine, Institute for Clinical and Experimental Medicine
- 700 1_
- $a Jíchová, Šárka $u Center for Experimental Medicine, Institute for Clinical and Experimental Medicine
- 700 1_
- $a Sadowski, Janusz $u Department of Renal and Body Fluid Physiology, Mossakowski Medical Research Institute, Polish Academy of Science, Warsaw, Poland
- 700 1_
- $a Kompanowska-Jezierska, Elzbieta $u Department of Renal and Body Fluid Physiology, Mossakowski Medical Research Institute, Polish Academy of Science, Warsaw, Poland
- 700 1_
- $a Walkowska, Agnieszka $u Department of Renal and Body Fluid Physiology, Mossakowski Medical Research Institute, Polish Academy of Science, Warsaw, Poland
- 700 1_
- $a Veselka, Josef $u Department of Cardiology, University Hospital Motol and 2nd Faculty of Medicine, Charles University, Prague, Czech Republic
- 700 1_
- $a Táborský, Miloš $u Department of Internal Medicine I, Cardiology, University Hospital Olomouc and Palacký University, Olomouc
- 700 1_
- $a Maxová, Hana $u Department of Pathophysiology, 2nd Faculty of Medicine, Charles University
- 700 1_
- $a Vaněčková, Ivana $u Institute of Physiology of the Czech Academy of Sciences, Prague, Czech Republic
- 700 1_
- $a Červenka, Luděk $u Center for Experimental Medicine, Institute for Clinical and Experimental Medicine $u Department of Internal Medicine I, Cardiology, University Hospital Olomouc and Palacký University, Olomouc
- 773 0_
- $w MED00002723 $t Journal of hypertension $x 1473-5598 $g Roč. 41, č. 1 (2023), s. 99-114
- 856 41
- $u https://pubmed.ncbi.nlm.nih.gov/36204993 $y Pubmed
- 910 __
- $a ABA008 $b sig $c sign $y p $z 0
- 990 __
- $a 20230120 $b ABA008
- 991 __
- $a 20230131150938 $b ABA008
- 999 __
- $a ok $b bmc $g 1891066 $s 1183402
- BAS __
- $a 3
- BAS __
- $a PreBMC-MEDLINE
- BMC __
- $a 2023 $b 41 $c 1 $d 99-114 $e 20221007 $i 1473-5598 $m Journal of hypertension $n J Hypertens $x MED00002723
- LZP __
- $a Pubmed-20230120