Linalool elicits vasorelaxation of mouse aortae through activation of guanylyl cyclase and K(+) channels.

OBJECTIVES: The aim of this study was to investigate the cardiovascular relaxing properties of monoterpene alcohol (-)-linalool (LIN), a principal component of several aromatic plants.
METHODS: We assessed the effects of LIN on vascular contractility in mouse aortae and evaluated its underlying mechanisms of action. KEY
FINDINGS: We found that LIN dose-dependently relaxed the vascular tonus of mouse thoracic aortae induced by prostaglandin F2 alpha (PGF2α , 3 μm). This effect, however, was reduced by pretreatment with the nitric oxide synthase inhibitor L-NAME (30 μm). Treatment with the inhibitor of soluble guanylyl cyclase ODQ (2 μm) or the K(+) channel blocker TEA (10 mM) partially blocked LIN-induced vasorelaxation. Moreover, addition of TEA after incubation of the rings with L-NAME and ODQ partially blocked LIN-induced vasorelaxation. Furthermore, LIN was able to partially antagonize CaCl2 -induced contractions in high potassium (80 mM) Krebs' solution, whereas LIN did not affect Ca(2+) release from endoplasmic reticulum Ca(2+) stores.
CONCLUSION: Our findings indicate that LIN may induce endothelium-dependent vasorelaxation in mouse thoracic aortae by activating soluble guanylyl cyclase and K(+) channels.