Apocynin improves endothelial function and prevents the development of hypertension in fructose fed rat

Abstract

Background and objectives: Exaggerated production of superoxide and inactivation of nitric oxide have been implicated in pathogenesis of hypertension. NAD(P)H oxidase is one of the major source of reactive oxygen species in vasculature. In the present study, we aimed to determine the effect of chronic administration of Apocynin an NAD(P)H oxidase inhibitor on endothelial function and hypertension in fructose-fed rat.

Materials and methods: Endothelial function, vascular superoxide, and nitric oxide production/bioavailability in aortas from fructose-fed rats and age-matched controls treated with or without apocynin were assessed using isometric tension studies in organ chambers. Systolic blood pressure was measured by the tail cuff method.

Results: In fructose-fed rats, acetylcholine-induced relaxation was impaired, vascular superoxide production was increased, and nitric oxide bioavailability was decreased along with an increase in systolic blood pressure compared to controls. Apocynin treatment prevented the increased generation of superoxide, decreased nitric oxide bioavailability, impaired acetylcholine-induced relaxation, and elevation of systolic blood pressure.

Conclusion: Chronic administration of apocynin improves the endothelial function by reducing oxidative stress, improving NO bioavailability, and prevents the development hypertension in fructose-fed rat.

Keywords: NAD(P)H oxidase; Superoxide; apocynin; endothelial dysfunction; hypertension; nitric oxide.

Figure 1

Systolic blood pressure in control and fructose fed-animals treated with or without apocynin. Control, control + apocynin, fructose fed, fructose + apocynin. **P < 0.01 F vs. C, **P < 0.01 FA vs. F

Figure 2

Acetylcholine-induced relaxation of isolated rat aorta preconstricted with phenylephrine in control and fructose-fed animals treated with or without apocynin. Control, control + apocynin, fructose fed, fructose + apocynin. *P < 0.05 F vs. C, *P < 0.05 FA vs. F

Figure 3

Sodium nitroprusside-induced relaxation of isolated rat aorta preconstricted with phenylephrine in control and fructose-fed animals treated with or without apocynin. Control, control + apocynin, fructose fed, fructose + apocynin

Figure 4

Super-oxide level measured as tempo-induced relaxation of isolated rat aorta preconstricted with phenylephrine in control and fructose-fed animals treated with or without apocynin. Control, control + apocynin, fructose fed, fructose + apocynin. **P < 0.01 F vs. C, **P < 0.01 FA vs. F

Figure 5

Nitric oxide level measured as L-NAME-induced contraction of isolated rat aorta preconstricted with phenylephrine in control and fructose-fed animals treated with or without apocynin. Control, control + apocynin, fructose fed, fructose + apocynin. *P < 0.05 F vs. C, *P < 0.05 FA vs. F