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BACKGROUND Coffee is a rich source of antioxidative polyphenols, but epidemiological studies and interventional trials have failed to demonstrate any clear beneficial effects of coffee consumption on hypertension. The interaction between hydroxyhydroquinone (HHQ) and 5-caffeoylquinic acid (CQA) was examined, in an attempt to understand the controversial effects of coffee on hypertension. METHODS Male Wistar Kyoto (WKY) rats or spontaneously hypertensive rats (SHRs, 14 weeks old) were divided into the following four groups; those on a control diet, 0.005% HHQ diet, 0.5% CQA diet, and HHQ plus CQA diet. The rats were fed the above diets for 8 weeks, and the tail arterial blood pressure was monitored in conscious rats at 2-week intervals. Urinary nitric oxide (NO) metabolites and hydrogen peroxide (H2O2) excretion were measured 8 weeks after the start of the experiment. Endothelium-dependent and -independent vasorelaxant responses and immunohistochemical staining for nitrotyrosine were examined in aortas. RESULTS HHQ inhibited the CQA-induced improvement in hypertension, urinary NO metabolites or H2O2 excretion, endothelial dysfunction, and nitrotyrosine deposits in aortas in SHR. However, the administration of HHQ alone had little effect on either strain. CONCLUSIONS Based on the content ratio of HHQ and chlorogenic acids in coffee, HHQ interfered with the CQA-induced improvement in blood pressure and endothelial function in SHR. The results explain, at least in part, the conflicting action of coffee drinking on hypertension and vascular reactivity. [ABSTRACT FROM AUTHOR]

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. [Copyright &y& Elsevier]