Contractile responses of helically-cut strips of the rabbit aorta to drugs, ions and transmural electrical stimulation were compared at different temperatures of the bathing medium, the response at 37 °C being taken as control. The dose-response curve of norepinephrine was moved to the right and downward by lowering the temperature from 37 to 25 °C and by raising temperature to 40 °C. Responses to transmural neural stimulation at frequencies of 5 and 20/sec were attenuated at 25 °C, the attenuation being greater in the response at the lower frequency. Concentrations of exogenous norepinephrine needed to produce the same magnitude of contraction as that with transmural stimulation were markedly increased by lowering the temperature to 25 °C. Contractile responses to norepinephrine (2 x 10<sup>-6</sup> m), histamine (2 × 10<sup>-5</sup> m) and angiotensin II (10<sup>-7</sup> m) were attenuated by 32–44% at 25 °C, whereas the responses to K<sup>+</sup> (25 mil) and Ba<sup>++</sup> (2 mil) were dependent on temperatures between 25 and 37 °C and were attenuated by 69 and 92%, respectively, at 25 °C. Contractures induced by Ca<sup>++</sup> in K<sup>+</sup>-depolarized preparations exposed to Ca<sup>++</sup>-free media and also by Ba<sup>++</sup> in preparations exposed to Ca<sup>++</sup>-free media varied directly by raising temperatures. Interference with the influx of divalent cations, such as Ca<sup>++</sup> and Ba<sup>++</sup>, may be involved in the cold inhibition of aortic contractility.