Proceedings of The Physiological Society

Europhysiology 2018 (London, UK) (2018) Proc Physiol Soc 41, PCA312

Poster Communications

Antihypertensive and antioxidative effects of whole grain essential oil in nitric oxide deficient hypertensive rats

G. Jan-on1,2, K. Senaphan3,2, W. Sangartit1,2, P. Pakdeechote1,2, V. Kukongviriyapan4, U. Kukongviriyapan1,2

1. Department of Physiology, Faculty of Medicine, Khon Kaen University, Khon kaen, Thailand. 2. Cardiovascular research group, Khon Kaen University, Khon kaen, Thailand. 3. Division of Physiology, Faculty of Veterinary Medicine, Khon Kaen University, Khon kaen, Thailand. 4. Department of Pharmacology, Faculty of Medicine, Khon Kaen University, Khon kaen, Thailand.


Hypertension is one of the major risk factors for cardiovascular disease (CVD). Nitric oxide (NO) plays an important role in the regulation of cardiovascular function. Inhibition of NO synthesis results in development of hypertension. Oxidative stress is associated with the pathogenesis of hypertension. Consumption of healthy diet that contains natural antioxidants appears to reduce blood pressure and may decrease risk for CVD. Whole grain essential oil (WEO) extracted from brown rice contains high levels of dietary antioxidants which may protect against diseases related to oxidative stress. Therefore, this study aimed to investigate the antihypertensive effect of WEO in NO deficient hypertensive rats. Hypertension was induced in male Sprague-Dawley rats (200-230 g, n=6/group) by receiving Nω-nitro-L-arginine methyl ester (L-NAME), a NO synthase inhibitor, at dose of 50 mg/kg/day in drinking water for 3 weeks. Simultaneously, L-NAME-treated rats were intragastrically administered daily with deionized water (DI) for untreated control group or WEO (1 or 2 ml/kg) for treated groups. Rats received tap water and intragastrically administered with DI were served as normotensive controls. At the end of experiment, rats were anaesthetized with an intraperitoneal injection of pentobarbital sodium (60 mg/kg). The left femoral artery and femoral vein were cannulated for continuously monitoring arterial blood pressure and for infusion of vasoactive agents, respectively. Rats were sacrificed by overdose of anaesthetic drug. Blood samples and thoracic aorta were collected for assay of oxidative stress markers. Data were expressed as means ± S.E.M., compared by ANOVA. Results showed that WEO significantly decreased arterial blood pressure of L-NAME-treated rats compared to normotensive controls (138.9 ± 5.8, 118.1 ± 3.7 vs. 160.4 ± 3.6 mmHg L-NAME control p<0.05). The vascular response to vasoconstrictor, phenylephrine (0.1 µM) was augmented while the response to endothelial-dependent vasodilator, acetylcholine (30 nM), was blunted in l-NAME-treated rats. WEO significantly improved the vascular responsiveness of L-NAME hypertensive rats (p<0.05). The antihypertensive effect of WEO was associated with a reduction in vascular superoxide production, plasma malondialdehyde and protein carbonyl (p<0.05). Moreover, WEO also increased eNOS expression and suppressed p47phox NADPH oxidase in the vascular tissues (p<0.05). The present results provide evidence for the antihypertensive and antioxidative properties of WEO and suggest that WEO might be useful as a dietary supplement against hypertension.

Where applicable, experiments conform with Society ethical requirements