RENAL FUNCTIONS/EETS

"Role of Epoxyeicosatrienoic Acids in the Regulation of Blood Pressure, Renal Hemodynamics and Sodium Excretion in Renovascular Model of Hypertension"

 Coordinatore Institut klinické a experimentální mediciny 

 Organization address address: Videnska 1958/9
city: PRAGUE 4
postcode: 14021

contact info
Titolo: Mr.
Nome: Tomas
Cognome: Linhart
Email: send email
Telefono: +42026136 2406
Fax: +42026136 2805

 Nazionalità Coordinatore Czech Republic [CZ]
 Totale costo 75˙000 €
 EC contributo 75˙000 €
 Programma FP7-PEOPLE
Specific programme "People" implementing the Seventh Framework Programme of the European Community for research, technological development and demonstration activities (2007 to 2013)
 Code Call FP7-PEOPLE-2009-RG
 Funding Scheme MC-IRG
 Anno di inizio 2009
 Periodo (anno-mese-giorno) 2009-10-01   -   2016-09-30

 Partecipanti

# participant  country  role  EC contrib. [€] 
1    Nome Ente NON disponibile

 Organization address address: Videnska 1958/9
city: PRAGUE 4
postcode: 14021

contact info
Titolo: Mr.
Nome: Tomas
Cognome: Linhart
Email: send email
Telefono: +42026136 2406
Fax: +42026136 2805

CZ (PRAGUE 4) coordinator 75˙000.00

Mappa


 Word cloud

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seh    hypertension    bp    pressure    regulation    cyp       renal    inhibition    eets    functions    attenuates    addition   

 Obiettivo del progetto (Objective)

'Cytochrome P450 (CYP) metabolites are more frequently recognized as important regulators of cardiovascular and renal functions. CYP epoxygenases produce epoxyeicosatrienoic acids (EETs) that exhibit vasodilatory and natriuretic properties. EETs are degraded by the enzyme soluble epoxide hydrolase (sEH). Inhibition of sEH increases the level of EETs and attenuates blood pressure (BP) and end organ damage in several models of hypertension. We would like to define the role of EETs in BP regulation in the model of renovascular two kidney one clip (2K1C) hypertension. We will examine whether sEH inhibition attenuates BP and improves renal autoregulation and pressure natriuresis in 2K1C hypertension. In addition, we will study the signaling of EETs in isolated renal arterioles to determine the changes in EETs - mediated signal transduction in hypertension. Overall, these studies could elucidate the role of EETs in the regulation of renal functions and BP under physiological conditions and in hypertension. In addition, these studies could provide new evidence supporting the role of sEH inhibitor as the new candidate for antihypertensive therapy.'

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