The objective was to define the spasmogenic properties of ethanol and its effects on vascular smooth muscle contractility, particularly with reference to the involvement of the prostaglandin system in such effects. A twelve channel bioassay system was set up to measure responses of rat aortic rings as well as other preparations using force/displacement transducers. Ethanol was introduced in vitro or through an inhalation model in vivo. Our results show a biphasic response to ethanol both in regard to the contractile response to a thromboxane mimic and to prostaglandin synthesis. Low doses of ethanol decreased contractility and markedly increased the PGI2/TXA2 ratio, whereas higher levels had no effect on contractility and decreased the PGI2/TXA2 ratio.