We studied vasomotor responses of aortic endothelium in a rat model of chronic smoking. It was found that long-term exposure to tobacco smoke (inhalation) impaired vasomotor function of the aortic endothelium leading to insufficient vasodilator activity and enhanced vasoconstriction. After the cessation of inhalations, vasomotor disturbances were not only preserved, but also exacerbated because of increased pathological endothelium-independent vasoconstriction.
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