Effect of 20-HETE inhibition on L-NAME-induced hypertension in rats
CLINICAL AND EXPERIMENTAL HYPERTENSION, vol.40, no.3, pp.292-302, 2018 (SCI-Expanded, Scopus)
- Publication Type: Article / Article
- Volume: 40 Issue: 3
- Publication Date: 2018
- Doi Number: 10.1080/10641963.2017.1368540
- Journal Name: CLINICAL AND EXPERIMENTAL HYPERTENSION
- Journal Indexes: Science Citation Index Expanded (SCI-EXPANDED), Scopus
- Page Numbers: pp.292-302
- Keywords: 20-HETE, blood pressure, HET-0016, L-NAME, vascular responsiveness, CHRONIC NOS INHIBITION, OXIDE-DEFICIENT HYPERTENSION, 20-HYDROXYEICOSATETRAENOIC ACID, NITRIC-OXIDE, ENDOTHELIAL DYSFUNCTION, VASCULAR REACTIVITY, BLOOD-PRESSURE, RESISTANCE ARTERIES, OMEGA-HYDROXYLASE, ARACHIDONIC-ACID
- Akdeniz University Affiliated: Yes
Abstract
20-Hydroxyeicosatetraenoicacid (20-HETE) is an important mediator that regulates vascular tone and blood pressure (BP). Although various experimental animal hypertension models demonstrated that 20-HETE contributes to increased vascular resistance and BP, these effects have not been studied in N-nitro-L-arginine methyl ester hydrochloride (L-NAME)-induced hypertension model. In this study, we investigated the effects of 20-HETE on the vascular responsiveness and BP in an L-NAME-induced hypertension.Wistar Albino rats were used in this study. Hypertension was induced by the addition of L-NAME to drinking water for 5weeks. The study was performed in three stages: first, BP changes were monitored in real time in the presence of 20-HETE enzymatic inhibitor, N-hydroxy-N-(4-butly-2-methylphenyl)-formamidine (HET-0016) for 1h. Second, vascular responses of the conduit and resistance arteries were investigated in the presence or absence of HET-0016 in the organ bath. Third, BP was monitored weekly in some hypertensive animals treated with HET-0016 and vascular responses were investigated at the end of the experiment.We demonstrated an increase in 20-HETE levels in the resistance arteries of hypertensive animals. 20-HETE inhibition by HET-0016 significantly decreased BP in L-NAME-induced hypertension model. In addition, HET-0016 treatment caused significant improvement in vascular dilator and constrictor responses in the conduit and resistance arteries.This study demonstrates an important role of 20-HETE in increasing BP and altering vascular responsiveness in L-NAME-induced hypertension model, which suggests a possible involvement of 20-HETE in essential hypertension development in humans.