Teramethylammonium(TMA) in one of the synthetic compounds of nicotine that act at ganglionic site. The major action of TMA consists of initial stimulation followed by a more persistent depression of all autonomic ganglia by binding to a cholinergic receptor. It is well believed that the level of membrane potential in arterial smooth muscle is an important regulator of tension development. Depolarization and hyperpolarization by only few millivolts results in significant changes in tension. In general, the agents of vascular smooth muscle induce vascular relaxaion. The present study was undertaken to elucidate the effect of TMA on vascular contractility in the isolated rabbit thoracic aorta with or without endothelial cell, and mechanisms involved in the change of vascular contractility by TMA. The results obtained are summarized as follows ; 1) In the presence of endothelial cell, TMA induced a relaxtion of the aorta precontracted with norepinephrine but induced a contraction in the aorta without endothelial cells, indicating that in the rabbit aorta, relaxations produced by TMA were the endothelium-dependent. 2) The addition of inhibitor such as methylene blue, hemoglobin, hydroquinone and p-bromophenacyl bromide during the TMA-induced relaxation reversed the contractile tension to a level similar to or higher than that before the addition of TMA in rabbit thoracic aorta.This relaxation effect of TMA suggest that the TMA-inducdd relaxation in rabbit aorta is due to the release of endotheline derived relaxing factor(EDRF). 3) Relaxation induced by TMA was antagonized by atropine and thus the TMA does seem to act on the muscarinic receptors. 4) TMA reduced the norepinephrine-induced Ca++ influx into rabbit smooth muscle membrane. From the above results, it may be concluded that TMA-induced vacular relaxation in rabbit aorta is due to the release of EDRF. Mechanism involved in the relaxation induced by TMA may be the stimulation of soluble guanylate cyclase and increased tissue cGMP concentrations.