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

Title:

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

Creator:

Luděk Červenka, Vojtěch Melenovský, Zuzana Husková, Sporková, A., Marcela Bürgelová, Petra Škaroupková, Hwang, S. H., Hammock, B. D., Imig, J. D., and Sadowski, J.

Identifier:

https://cdk.lib.cas.cz/client/handle/uuid:23bdf7fd-7b29-4778-a223-97c597eceb65
uuid:23bdf7fd-7b29-4778-a223-97c597eceb65
issn:0862-8408

Subject:

Fyziologie člověka a srovnávací fyziologie, fyziologie, physiology, congestive heart failure, aorto-caval fistula, renin-angiotensin system, epoxyeicosatrienoic acids, soluble epoxide hydrolase, 14, and 612

Type:

article, články, model:article, and TEXT

Format:

print, bez média, and svazek

Description:

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 m yocardial 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 o verload. 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., L. Červenka, V. Melenovský, Z. Husková, A. Sporková, M. Bürgelová, P. Škaroupková, S. H. Hwang, B. D. Hammock, J. D. Imig, J. Sadowski., and Obsahuje bibliografii

Language:

English

Rights:

http://creativecommons.org/licenses/by-nc-sa/4.0/
policy:public

Source:

Physiological research | 2015 Volume:64 | Number:6

Harvested from:

CDK

Metadata only:

false