Antihypertensive activity of Rosa rugosa Thunb. flowers: Angiotensin I converting enzyme inhibitor

Abstract

Ethnopharmacological relevanceRosa rugosa Thunb.'s flowers have been used for medicinal and food purposes for hundreds years in China. They have been used in Traditional Chinese Medicine (TCM) to effectively help in expansion of blood vessels and improvement of microcirculation. Current high prevalence of hypertension, and the associated side effects of synthetic Angiotensin I converting enzyme inhibitors usually prescribed for this condition, led us to the investigation of possible inhibitory activity of the Rosa rugosa Thunb. flower extracts on Angiotensin I converting enzyme (ACE). Materials and methodsTwo different extraction preparation: (1) powdered materials were extracted with water (RW) and then with water (RWW), ethyl acetate (RWE) and 95% ethanol (RWE95); (2) powdered materials were extracted with 95% ethanol (RE95) and then with water (RE95W), ethyl acetate (RE95E) and 95% ethanol (RE95E95). The inhibition activity was determined using in vitro the inhibitory effect on Angiotensin I converting enzyme (ACE), and using the acute response and chronic response on blood pressure which measured in spontaneously hypertensive rats (SHRs). ResultsBoth RE95E95 and RWW had highest ACE inhibitor activities. The higher inhibitor activity of RE95E95 was also evaluated in SHRs by oral administration for antihypertensive effect. In acute experiment, the decrease in systolic blood pressure (SBP) and the increase in heart rate (HR) was observed at 2h after administration at high (40g/kg) and low (20g/kg) dose; such reductions in SBP were maintained for 12h. Low dose had reduced SBP significantly more than high dose. In multiple oral administration chronic experiment, a SBP reduction of 17.5mmHg was observed after 6d administration at low dose, and such reductions were maintained for the next 8 days. ConclusionsThe experimental results demonstrated the antihypertensive effect of Rosa rugosa Thunb. flowers, which was attributed to inhibition of Angiotensin I converting enzyme.