Endothelium-dependent vasodilation by ferulic acid in aorta from chronic renal hypertensive rats.
- Author:
Seok CHOI
1
;
Hyun Il KIM
;
Sang Hag PARK
;
Mi Jung LEE
;
Jae Yeoul JUN
;
Hyun Lee KIM
;
Jong Hoon CHUNG
;
Cheol Ho YEUM
Author Information
1. Department of Physiology, College of Medicine, Chosun University, Gwangju, Korea. chyum@chosun.ac.kr
- Publication Type:Original Article
- Keywords:
Endothelium;
Ferulic acid;
Renal hypertension;
Vasodilation
- MeSH:
Animals;
Aorta;
Aorta, Thoracic;
Baths;
Biological Availability;
Coumaric Acids;
Endothelium;
Hydroquinones;
Hypertension;
Hypertension, Renal;
NG-Nitroarginine Methyl Ester;
Nitric Oxide;
Nitric Oxide Synthase;
Phenylephrine;
Placebos;
Rats;
Relaxation;
Renal Artery;
Salicylamides;
Vasodilation
- From:Kidney Research and Clinical Practice
2012;31(4):227-233
- CountryRepublic of Korea
- Language:English
-
Abstract:
BACKGROUND: Ferulic acid (FA) is a naturally occurring nutritional compound. Although it has been shown to have antihypertensive effects, its effects on vascular function have not been intensively established. The aim of this study was to assess the vasoreactivity of FA in chronic two-kidney, one-clip (2K1C) renal hypertensive rats. METHODS: Hypertension was induced in 2K1C rats by clipping the left renal artery and age-matched rats that received a sham treatment served as a control. Thoracic aortas were mounted in tissue baths to measure isometric tension. The effects of FA on vasodilatory responses were evaluated based on contractile responses induced by phenylephrine in the aortic rings obtained from both 2K1C and sham rats. Basal nitric oxide (NO) bioavailability in the aorta was determined by the contractile response induced by NO synthase inhibitor NG-nitro-L-arginine methyl ester (L-NAME). RESULTS: FA induced concentration-dependent relaxation responses which were greater in 2K1C hypertensive rats than in sham-clipped control rats. This relaxation induced by FA was partially blocked by the removal of endothelium or by pretreating with L-NAME. L-NAME-induced contractile responses were augmented by FA in 2K1C rats, while no significant differences were noted in sham rats. FA improved acetylcholine-induced endothelium-dependent vasodilation in 2K1C rats, but not in sham rats. The simultaneous addition of hydroxyhydroquinone significantly inhibited the increase in acetylcholine-induced vasodilation by FA. CONCLUSION: These results suggest that FA restores endothelial function by altering the bioavailability of NO in 2K1C hypertensive rats. The results explain, in part, the mechanism underlying the vascular effects of FA in chronic renal hypertension.
