Proceedings of The Physiological Society

Europhysiology 2018 (London, UK) (2018) Proc Physiol Soc 41, PCA313

Poster Communications

Rice bran hydrolysates lower blood pressure and improve vascular function in L-NAME-induced hypertensive rats

K. Senaphan1,2, S. Chumjit3,2, W. Sangartit3,2, V. Kukongviriyapan4, S. Thawornchinsombut5,2, U. Kukongviriyapan3,2, T. ProongKhong6, R. Changsri6

1. Division of Physiology, Faculty of Veterinary Medicine, Khon Kaen University, Khon Kaen, Thailand. 2. Cardiovascular Research Group, Khon Kaen University, Khon Kaen, Thailand. 3. Department of Physiology, Faculty of Medicine, Khon Kaen University, Khon Kaen, Thailand. 4. Department of Pharmacology, Faculty of Medicine, Khon Kaen University, Khon Kaen, Thailand. 5. Department of Food Technology, Faculty of Technology, Khon Kaen University, Khon Kaen, Thailand. 6. Chum Phae Rice Research Center, Khon Kaen, Thailand.

Hypertension is an important public health problem worldwide. Numerous experimental models of hypertension have been developed and Nω-nitro-L-arginine methyl ester (L-NAME)-induced hypertension is a well established model. Inhibition of nitric oxide (NO) synthesis with L-NAME induces a marked increase of blood pressure, endothelial dysfunction and oxidative stress. This model is useful for studying the influences of oxidative stress, NO deficiency and also evaluating antihypertensive agents. Tubtim Chum Phae rice, a new breed of red pericarp rice, is a hybrids of mixed Hom Mali rice and Sang Yhod rice. Rice bran hydrolysates extracted from Tubtim Chum Phae defatted rice bran (TCRH) consist of bioactive compounds with high antioxidant activities. This study aimed to investigate whether TCRH could reduce blood pressure, ameliorate endothelial dysfunction and oxidative stress in L-NAME-induced hypertensive rats. Male Sprague-Dawley rat (180-220 g, n=30) were randomly divided into 5 groups (n=6): control+deionized water (DI), control+TCRH 500 mg/kg, L-NAME+DI, L-NAME+TCRH 250 mg/kg,and L-NAME+TCRH 500 mg/kg. The control group received tap water and the L-NAME-treated group received L-NAME (50 mg/kg/day) in drinking water for 3 weeks. TCRH (250 or 500 mg/kg/day) or DI, as a vehicle was fed to rats simultaneously with L-NAME. At the end of experiment, rats were anesthetized with pentobarbital sodium (60 mg/kg, i.p.). The left femoral artery was cannulated for monitoring arterial blood pressure. Hindlimb blood flow (HBF) was measured by placing electromagnetic flow probes around the abdominal aorta and hindlimb vascular resistance (HVR) was calculated from the mean arterial pressure (MAP) and HBF. Vascular reactivity was evaluated by infusing acetylcholine (10 nmol/kg) through an additional catheter in the femoral vein. Blood samples and aortic tissues were collected for biochemical and protein expression analyses. Values are means ± S.E.M., compared by ANOVA. TCRH at both concentrations significantly reduced arterial blood pressure (174±1.4, 156±2.9 vs.194±3.9 mmHg L-NAME controls, p<0.05) and vascular resistance. The vascular responses to acetylcholine of L-NAME rats-treated with TCRH were significantly increased (40±0.8, 49±0.1 vs.31±0.9 % L-NAME controls, p<0.05). The reduction in blood pressure was associated with a decrease in plasma angiotensin-converting enzyme activity and an increase in plasma nitrate/nitrite and eNOS protein expression. TCRH also reduced plasma malonaldehyde and increased blood glutathione level. The overall findings suggest that TCRH exhibits an antihypertensive effect via its antioxidant capacity and vasodilatory property.

Where applicable, experiments conform with Society ethical requirements