Planta Med 2013; 79 - PB42
DOI: 10.1055/s-0033-1351987

Crataegus special extract WS® 1442 ameliorates angiotensin II-induced endothelial dysfunction in rats

E Schramm 1, E Koch 1
  • 1 Dr. Willmar Schwabe GmbH & Co. KG, Preclinical Research, 76227 Karlsruhe, Germany

Impaired endothelium-dependent relaxation is a characteristic hallmark of most cardiovascular disorders such as hypertension, atherosclerosis, coronary/peripheral artery disease or chronic heart failure. Indeed, endothelial dysfunction (ED) has been shown to be of prognostic value in predicting vascular events including stroke and myocardial infarction. A major cause for diminished vasodilatory responses is a reduced endothelial generation of nitric oxide (NO) or its accelerated degradation due to oxidative excess.

WS® 1442 is a dry extract from hawthorn (Crataegus ssp.) leaves with flowers that previously has been reported to induce endothelium-dependent NO-mediated relaxations of porcine coronary artery rings through a stimulation of endothelial nitric oxide synthase (eNOS). It was the aim of the present study to evaluate whether intake of WS® 1442 is also able to prevent ED in vivo. For this purpose, ED was induced in male Wistar rats by infusion of angiotensin II (Ang II, 0.4 mg/kg/day) for a period of 14 days using implanted osmotic minipumps. WS® 1442 (about 300 mg/kg/day) was administered via enriched feed for one week before and during the Ang II infusion. Following euthanasia reactivity of the isolated aorta was assessed by relaxation of the phenylephrine-precontracted vessel to increasing concentrations of acetylcholine. In addition, the total oxidative capacity, prorenin/renin concentration, and renin activity were determined in the plasma.

Ang II infusion induced an impaired relaxation of the aorta and decreased renin activity which were almost completely or partially normalized by treatment with WS® 1442. However, WS® 1442 had no effect on the decreased oxidative capacity and the reduced prorenin/renin concentration. In conclusion, the present findings indicate that intake of WS® 1442 improves Ang II-induced ED in rats. This protective effect is most probably due to an enhanced endothelial formation of NO following activation of eNOS.