Effect of 20-HETE inhibition on L-NAME-induced hypertension in rats

ÖZEN N., ULKER S. N., ULKER P., Ozcan F., Aslan M., Senturk U. K., ...Daha Fazla

CLINICAL AND EXPERIMENTAL HYPERTENSION, cilt.40, sa.3, ss.292-302, 2018 (SCI-Expanded) identifier identifier identifier

  • Yayın Türü: Makale / Tam Makale
  • Cilt numarası: 40 Sayı: 3
  • Basım Tarihi: 2018
  • Doi Numarası: 10.1080/10641963.2017.1368540
  • Dergi Adı: CLINICAL AND EXPERIMENTAL HYPERTENSION
  • Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus
  • Sayfa Sayıları: ss.292-302
  • Anahtar Kelimeler: 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 Üniversitesi Adresli: Evet

Özet

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.