Schisandra chinensis (SC) is a known medical herb for the treatment of cardiovascular
symptoms associated with menopausal symptoms in Korea. However, the pharmacological
action mechanisms involved have not been well studied. This study was aimed to investigate
the vascular effects of SC in rat thoracic aorta.
We isolated the hexane, chloroform, and methanol extracts from SC and evaluated their
vasodilatory effects in the rat thoracic aorta.
Hexane extracts of SC (SCHE, 5 x 10(-5) to 10(-3) g/L) caused a concentration-dependent
relaxation in both endothelium-intact and -denuded aortas. The relaxant effect of
SCHE on the endothelium-intact aorta was more prominent than on the endothelium-denuded
aorta. The former was significantly attenuated by L-NAME, a nitric oxide synthase
inhibitor, and ODQ, a soluble guanyl cyclase inhibitor, but not by tetraethylammonium,
a nonselective blocker of K(+) channels, and indomethacin, a cyclooxygenase inhibitor.
Furthermore, SCHE caused nitrite production as well as eNOS activation in aortic segments,
suggesting implication of NO signal pathway in SCHE-induced relaxation. In endothelium-denuded
aorta, SCHE-induced vasorelaxation was also attenuated by calyculin A, an inhibitor
of myosin light chain (MLC) phosphatase, but not by ML-9, a MLC kinase inhibitor,
suggestive of implication of MLC phosphatase activation. Phenylephrine-enhanced MLC
phosphorylation ratio was significantly attenuated by SCHE, which was recovered to
the control level by pretreatment with calyculin A.
Taken collectively, these findings suggest that the vascular relaxation evoked by
SCHE was mediated by not only endothelium dependent NO pathway but also direct effect
on vascular smooth muscle cell via dephosphorylation of MLC.