Detail
Článek
Článek online
FT
Medvik - BMČ
  • Je něco špatně v tomto záznamu ?

Inhibition of soluble epoxide hydrolase does not improve the course of congestive heart failure and the development of renal dysfunction in rats with volume overload induced by aorto-caval fistula

L. Červenka, V. Melenovský, Z. Husková, A. Sporková, M. Bürgelová, P. Škaroupková, S. H. Hwang, B. D. Hammock, J. D. Imig, J. Sadowski

. 2015 ; 64 (6) : 857-873. [pub] 2015Jun05

Jazyk angličtina Země Česko

Typ dokumentu časopisecké články

Perzistentní odkaz   https://www.medvik.cz/link/bmc16031122

Grantová podpora
NT14050 MZ0 CEP - Centrální evidence projektů
NT14012 MZ0 CEP - Centrální evidence projektů

The detailed mechanisms determining the course of congestive heart failure (CHF) and associated renal dysfunction remain unclear. In a volume overload model of CHF induced by creation of aorto-caval fistula (ACF) in Hannover Sprague-Dawley (HanSD) rats we explored the putative pathogenetic contribution of epoxyeicosatrienoic acids (EETs), active products of CYP-450 dependent epoxygenase pathway of arachidonic acid metabolism, and compared it with the role of the renin-angiotensin system (RAS). Chronic treatment with cis-4-[4-(3-adamantan-1-yl-ureido) cyclohexyloxy]benzoic acid (c-AUCB, 3 mg/l in drinking water), an inhibitor of soluble epoxide hydrolase (sEH) which normally degrades EETs, increased intrarenal and myocardial EETs to levels observed in sham-operated HanSD rats, but did not improve the survival or renal function impairment. In contrast, chronic angiotensin-converting enzyme inhibition (ACEi, trandolapril, 6 mg/l in drinking water) increased renal blood flow, fractional sodium excretion and markedly improved survival, without affecting left ventricular structure and performance. Hence, renal dysfunction rather than cardiac remodeling determines long-term mortality in advanced stage of CHF due to volume overload. Strong protective actions of ACEi were associated with suppression of the vasoconstrictor/sodium retaining axis and activation of vasodilatory/natriuretic axis of the renin-angiotensin system in the circulating blood and kidney tissue.

Citace poskytuje Crossref.org

000      
00000naa a2200000 a 4500
001      
bmc16031122
003      
CZ-PrNML
005      
20191108133813.0
007      
ta
008      
161101s2015 xr d f 000 0|ENG||
009      
AR
024    7_
$a 10.33549/physiolres.932977 $2 doi
035    __
$a (PubMed)26047375
040    __
$a ABA008 $b cze $d ABA008 $e AACR2
041    0_
$a ENG
044    __
$a xr
100    1_
$a Červenka, Luděk, $u Department of Pathophysiology, Second Faculty of Medicine, Charles University, Prague, Czech Republic; Center for Experimental Medicine, Institute for Clinical and Experimental Medicine, Prague, Czech Republic $d 1967- $7 xx0037105
245    10
$a Inhibition of soluble epoxide hydrolase does not improve the course of congestive heart failure and the development of renal dysfunction in rats with volume overload induced by aorto-caval fistula / $c L. Červenka, V. Melenovský, Z. Husková, A. Sporková, M. Bürgelová, P. Škaroupková, S. H. Hwang, B. D. Hammock, J. D. Imig, J. Sadowski
520    9_
$a The detailed mechanisms determining the course of congestive heart failure (CHF) and associated renal dysfunction remain unclear. In a volume overload model of CHF induced by creation of aorto-caval fistula (ACF) in Hannover Sprague-Dawley (HanSD) rats we explored the putative pathogenetic contribution of epoxyeicosatrienoic acids (EETs), active products of CYP-450 dependent epoxygenase pathway of arachidonic acid metabolism, and compared it with the role of the renin-angiotensin system (RAS). Chronic treatment with cis-4-[4-(3-adamantan-1-yl-ureido) cyclohexyloxy]benzoic acid (c-AUCB, 3 mg/l in drinking water), an inhibitor of soluble epoxide hydrolase (sEH) which normally degrades EETs, increased intrarenal and myocardial EETs to levels observed in sham-operated HanSD rats, but did not improve the survival or renal function impairment. In contrast, chronic angiotensin-converting enzyme inhibition (ACEi, trandolapril, 6 mg/l in drinking water) increased renal blood flow, fractional sodium excretion and markedly improved survival, without affecting left ventricular structure and performance. Hence, renal dysfunction rather than cardiac remodeling determines long-term mortality in advanced stage of CHF due to volume overload. Strong protective actions of ACEi were associated with suppression of the vasoconstrictor/sodium retaining axis and activation of vasodilatory/natriuretic axis of the renin-angiotensin system in the circulating blood and kidney tissue.
650    _2
$a kyselina 8,11,14-eikosatrienová $x analogy a deriváty $x krev $x metabolismus $7 D015126
650    _2
$a angiotensin I $x krev $7 D000803
650    _2
$a angiotensin II $x krev $7 D000804
650    _2
$a inhibitory ACE $7 D000806
650    _2
$a zvířata $7 D000818
650    _2
$a benzoáty $x farmakologie $x terapeutické užití $7 D001565
650    _2
$a modely nemocí na zvířatech $7 D004195
650    _2
$a preklinické hodnocení léčiv $7 D004353
650    _2
$a epoxid hydrolasy $x antagonisté a inhibitory $7 D004851
650    _2
$a epoxidové sloučeniny $x metabolismus $7 D004852
650    _2
$a srdeční selhání $x krev $x komplikace $x farmakoterapie $x ultrasonografie $7 D006333
650    _2
$a ledviny $x metabolismus $7 D007668
650    _2
$a mužské pohlaví $7 D008297
650    _2
$a myokard $x metabolismus $7 D009206
650    _2
$a peptidové fragmenty $x krev $7 D010446
650    _2
$a náhodné rozdělení $7 D011897
650    _2
$a krysa rodu Rattus $7 D051381
650    _2
$a renální insuficience $x krev $x etiologie $x prevence a kontrola $7 D051437
650    _2
$a renin-angiotensin systém $x účinky léků $7 D012084
650    _2
$a močovina $x analogy a deriváty $x farmakologie $x terapeutické užití $7 D014508
655    _2
$a časopisecké články $7 D016428
700    1_
$a Melenovský, Vojtěch $7 xx0160847 $u Department of Cardiology, Institute for Clinical and Experimental Medicine, Prague, Czech Republic
700    1_
$a Husková, Zuzana, $d 1978- $7 xx0074206 $u Center for Experimental Medicine, Institute for Clinical and Experimental Medicine, Prague, Czech Republic
700    1_
$a Sporková, Alexandra. $7 xx0239945 $u Center for Experimental Medicine, Institute for Clinical and Experimental Medicine, Prague, Czech Republic
700    1_
$a Bürgelová, Marcela, $d 1967- $7 xx0160368 $u Center for Experimental Medicine, Institute for Clinical and Experimental Medicine, Prague, Czech Republic
700    1_
$a Škaroupková, Petra $7 xx0117683 $u Center for Experimental Medicine, Institute for Clinical and Experimental Medicine, Prague, Czech Republic
700    1_
$a Hwang, S. H. $u Department of Entomology and UCD Comprehensive Cancer Center, University of California, Davis, California, USA
700    1_
$a Hammock, B. D. $u Department of Entomology and UCD Comprehensive Cancer Center, University of California, Davis, California, USA
700    1_
$a Imig, J. D. $u Department of Pharmacology and Toxicology, Medical College of Wisconsin, Wisconsin, USA
700    1_
$a Sadowski, Janusz, $d 1937- $u Department of Renal and Body Fluid Physiology, Mossakowski Medical Research Centre, Polish Academy of Science, Warsaw, Poland $7 xx0227641
773    0_
$w MED00003824 $t Physiological research $x 1802-9973 $g Roč. 64, č. 6 (2015), s. 857-873
856    41
$u http://www.biomed.cas.cz/physiolres/ $y domovská stránka časopisu
910    __
$a ABA008 $b A 4120 $c 266 $y 4 $z 0
990    __
$a 20161101 $b ABA008
991    __
$a 20191108134046 $b ABA008
999    __
$a ok $b bmc $g 1172209 $s 955780
BAS    __
$a 3
BAS    __
$a PreBMC
BMC    __
$a 2015 $b 64 $c 6 $d 857-873 $e 2015Jun05 $i 1802-9973 $m Physiological research $n Physiol. Res. (Print) $x MED00003824
GRA    __
$a NT14050 $p MZ0
GRA    __
$a NT14012 $p MZ0
LZP    __
$b NLK118 $a Pubmed-20161101

Najít záznam

Citační ukazatele

Možnosti archivace