Mechanism of vasorelaxation induced by Achillea wilhelmsii in rat isolated thoracic aorta

Achillea wilhelmsii (A. wilhelmsii) is used in Iraninan folk medicine for the treatment of hypertension; also, in previous reports, the hypotensive and antihypertensive effects of this plant have been indicated. The aim of the present study is to investigate the vasorelaxant effect of the hydroalcholic extract of A. wilhelmsii and its underlying mechanisms in isolated rat aorta.

The effect of the hydroalcholic A. wilhelmsii extract was tested on the contractile response of Wistar rat aorta induced by potassium chloride (KCl) and phenylephrine (PE) using a pressure transducer that is connected to the PowerLab.

The cumulative concentrations of A. wilhelmsii (0.5-8 mg/ml) induced a vasorelaxation both in endothelium-intact and endothelium-denuded aortas precontracted by high K+ (6 × 10−2 M) or 10−6 M PE. A. wilhelmsii, at a concentration of 4 mg/ml, reduced Ca2+-induced contraction (P < 0.001 vs. control) after PE or KCl had generated a stable contraction in the Ca2+-free solution. Furthermore, after incubation with diltiazem, the vasorelaxant effect of A. wilhelmsii reduced in the endothelium-denuded aortas precontracted by PE or KCl (P < 0.001 vs. control). In contrast, A. wilhelmsii-induced relaxation was not affected by glibenclamide, BaCl2 , ruthenium red, methylene blue, or heparin.

The results showed that A. wilhelmsii had a vasorelaxation effect, which was not endotheliumdependent. The relaxation was mediated by inhibition of extracellular Ca2+ influx through voltage- and receptor-operated Ca2+ channels (VDDCs and ROCCs) in vascular smooth muscle cells.