The role of endothelial nitric oxide in contractions induced by endogenous noradrenaline released by transmural nerve stimulation (TNS) and by exogenous noradrenaline (NA) was studied in isolated rings of rabbit carotid artery during cooling. At 37 degrees C, TNS produced frequency-dependent contractions of artery. Endothelium removal or inhibition of nitric oxide synthase by NG-nitro-L-arginine methyl ester (L-NAME) significantly enhanced TNS-induced contractions. The magnitude of maximal contraction to exogenous NA was increased in L-NAME-treated intact rings. Cooling the incubation bath from 37 degrees C to 26 degrees C increased the magnitude of neurogenic contractions in intact rings. L-NAME increased further the magnitude of neurogenic contractions at 26 degrees C in intact, but not in denuded arterial rings. Similarly, L-NAME increased contractions induced by exogenous NA during cooling. The results suggest that the response of the carotid artery to noradrenergic stimulation is modulated by nitric oxide originating from endothelial cells at normal as well as reduced temperature. (Tab. 1, Fig. 6, Ref. 19.)