Ferulic acid restores endothelium-dependent vasodilation in aortas of spontaneously hypertensive rats.
BACKGROUND
Ferulic acid (FA), a phytochemical constituent, has antihypertensive effects, but a detailed understanding of its effects on vascular function remains unclear. The vasoreactivity of FA was assessed using aortic rings isolated from normotensive Wistar Kyoto (WKY) and spontaneously hypertensive rats (SHR).


METHODS
The effects of FA (10(-5) to 10(-3) mol/L) on vasodilatory responses were evaluated based on contractile responses induced by phenylephrine (10(-6) mol/L) in thoracic aortic rings from male WKY rats and SHR. Basal nitric oxide (NO) bioavailability in the aorta was determined from the contractile response induced by the NO synthase inhibitor N(G)-nitro-L-arginine methyl ester (L-NAME, 10(-4) mol/L). The effects of FA on the production of NADPH-dependent superoxide anion were examined in SHR aortas. The impact of hydroxyhydroquinone, a generator of superoxide anions, on the FA-induced enhancement in acetylcholine-stimulated vasodilation was also investigated.


RESULTS
The FA (10(-3) mol/L)-induced relaxation was partially blocked by removal of the endothelium or by pretreating SHR aortas with L-NAME. FA increased NO bioavailability, and decreased NADPH-dependent superoxide anion levels in SHR aortas. Ferulic acid improved acetylcholine-induced endothelium-dependent vasodilation in SHR, but not in WKY. Furthermore, the simultaneous addition of hydroxyhydroquinone significantly inhibited the increase in acetylcholine-induced vasodilation by FA.


CONCLUSIONS
Ferulic acid restores endothelial function through enhancing the bioavailability of basal and stimulated NO in SHR aortas. The results explain, in part, the mechanisms underlying the effects of FA on blood pressure (BP) in SHR.
Suzuki
Atsushi
A
Biological Science Laboratories, Kao Corporation, Akabane Ichikai-machi, Tochigi, Tokyo, Japan. suzuki.atsushi2@kao.co.jp
Yamamoto
Masaki
M
Jokura
Hiroko
H
Fujii
Akihiko
A
Tokimitsu
Ichiro
I
Hase
Tadashi
T
Saito
Ikuo
I
D000109:Acetylcholine / Q000378:metabolism; D000818:Animals; D000959:Antihypertensive Agents / Q000494:pharmacology*; D001011:Aorta / Q000166:cytology / Q000187:drug effects; D003373:Coumaric Acids / Q000494:pharmacology*; D006152:Cyclic GMP / Q000378:metabolism; D004730:Endothelium, Vascular / Q000187:drug effects* / Q000503:physiopathology; D006873:Hydroquinones / Q000494:pharmacology; D006973:Hypertension / Q000139:chemically induced / Q000503:physiopathology*; D008297:Male; D009249:NADP / Q000494:pharmacology; D019331:NG-Nitroarginine Methyl Ester / Q000494:pharmacology; D051381:Rats; D011918:Rats, Inbred SHR; D011921:Rats, Inbred WKY; D013481:Superoxides / Q000378:metabolism; D013929:Thromboxane B2 / Q000378:metabolism; D014664:Vasodilation
D000959:Antihypertensive Agents; D003373:Coumaric Acids; D006873:Hydroquinones; D013481:Superoxides; C013038:hydroxyhydroquinone; D009249:NADP; D013929:Thromboxane B2; C004999:ferulic acid; D006152:Cyclic GMP; D000109:Acetylcholine; D019331:NG-Nitroarginine Methyl Ester