Acoustic rhinometry measures the cross-sectional area of the nasal cavity based on changes in acoustic impedance. The volume of the nasal cavity can be calculated by mathematical integration of the cross-sectional areas. One of the advantages of this procedure is that repeated measurements can be quickly performed non-invasively. In this study, we analyzed the mechanisms of nasal mucosal decongestion after applying vasoactive agents. The experiments were performed in normal adult volunteers (17 males, 3 females) who gave their informed consent to participate in this study. Three vasoactive agents (0.1% epinephrine, 0.5% phenylephrine hydrochloride, 0.5% oxymetazoline hydrochloride), two alpha-receptor antagonists (0.2% phenoxybenzamine, 0.4% yohimbine) and a local anesthetic (4% lidocaine) were used. In order to apply the agents precisely and safely, we attached a 6mm diameter disc moistened with 0.1 ml of solution to the anterior portion of the inferior turbinate unilaterally for fifty seconds. After removing the disc, acoustic measurements were performed for an hour. To analyze data we divided the nasal cavity into three portions, i.e., anterior, middle and posterior. Volume changes in each portion are expressed as percentages. Immediately after applying phenylephrine and oxymetazoline, ipsilateral volume in the anterior portion began to increase, and then extended posteriorly. The level of decongestion remained unchanged for an hour. Contralateral volume decreased in all portions. When epinephrine was applied, mucosal decongestion occurred first followed by congestion in all portions of the ipsilateral side after 20 minutes. Mucosal congestion occurred in all portions of the contralateral side. After applying phenoxybenzamine or yohimbine for ten minutes, we administered vasoactive agents topically. Pretreatment with alpha-1 antagonist almost totally suppressed the mucosal decongestion caused by phenylephrine and oxymetazoline. Contralateral congestion was decreased by antagonizing the suppression of ipsilateral decongestion. After application of lidocaine for ten minutes, phenylephrine still caused ipsilateral decongestion only in the anterior portion, but decongestion of the middle and posterior portion and congestion on the contralateral side totally disappeared. These findings suggest the following conclusions: 1) decongestion evoked by adrenergic agents is probably caused by direct activation of alpha-1 receptors, 2) decongestion of the middle and posterior portions is evoked by drug particles conveyed by ciliary movement, and 3) the contralateral response is probably related to the activation of sensory nerves on the ipsilateral side.