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. Fields of science natural scienceschemical sciencesinorganic chemistryalkali metalsnatural sciencesbiological sciencesbiochemistrybiomoleculesproteinsenzymes Programme(s) FP7-PEOPLE - Specific programme "People" implementing the Seventh Framework Programme of the European Community for research, technological development and demonstration activities (2007 to 2013) Topic(s) FP7-PEOPLE-2009-RG - Marie Curie Action: "Reintegration Grants" Call for proposal FP7-PEOPLE-2009-RG See other projects for this call Funding Scheme MC-IRG - International Re-integration Grants (IRG) Coordinator Institut klinické a experimentální mediciny EU contribution € 75 000,00 Address Videnska 1958/9 14021 Prague 4 Czechia See on map Region Česko Praha Hlavní město Praha Activity type Research Organisations Administrative Contact Tomas Linhart (Mr.) Links Contact the organisation Opens in new window Website Opens in new window Total cost No data
