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

Abstract

ObjectivesThe aim of this study was to investigate the cardiovascular relaxing properties of monoterpene alcohol (-)-linalool (LIN), a principal component of several aromatic plants. MethodsWe assessed the effects of LIN on vascular contractility in mouse aortae and evaluated its underlying mechanisms of action. Key findingsWe found that LIN dose-dependently relaxed the vascular tonus of mouse thoracic aortae induced by prostaglandin F-2 alpha (PGF(2), 3m). This effect, however, was reduced by pretreatment with the nitric oxide synthase inhibitor L-NAME (30m). Treatment with the inhibitor of soluble guanylyl cyclase ODQ (2m) or the K+ channel blocker TEA (10mM) 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 (80mM) Krebs' solution, whereas LIN did not affect Ca2+ release from endoplasmic reticulum Ca2+ stores. ConclusionOur findings indicate that LIN may induce endothelium-dependent vasorelaxation in mouse thoracic aortae by activating soluble guanylyl cyclase and K+ channels.