Cooling augments human saphenous vein reactivity to electrical stimulation

Human saphenous veins were obtained at operation and assayed immediately (n = 10). The veins were cut into rings, suspended in organ chambers, and connected to force transducers for recording of isometric tension. One ring served as control; others were treated with either the alpha 1-adrenoceptor antagonist prazosin (Pz, 3 x 10(-7) M) or the alpha 2-adrenoceptor antagonist rauwolscine (Rw1, 10(-7) M). Cooling from 37 degrees to 24 degrees C had no significant effect on the resting tone of quiescent rings. Electrical stimulation (0.2-16 Hz) caused frequency-dependent contractions in control vessels. The contractions were inhibited by Pz (p < 0.001) and by Rw (p < 0.001). In control rings, cooling potentiated contractions evoked at all frequencies. Similar augmentations were induced by cooling in rings treated with the alpha 1-antagonist Pz. In contrast, rings treated with Rw before being electrically stimulated showed no significant change in contractile force when cooled. The data indicate that in the human saphenous vein, both alpha 1- and alpha 2-adrenoceptors are innervated, contributing to contractile response evoked by neuronal excitation. Cold augments saphenous vein reactivity to endogenously released norepinephrine (NE) by an apparent increase in the responsiveness of alpha 2-adrenoceptors to agonists. This relationship between temperature and adrenoceptor responsiveness is consistent with the hypothesized role of alpha 2-adrenoceptors in cold-induced vasospasm.