The effects of cooling on human saphenous vein reactivity to adrenergic agonists

Human saphenous veins were obtained at surgery and assayed immediately (n = 10). The veins were cut into rings, suspended in organ chambers, and connected to force transducers for the recording of isometric tension. One ring served as control whereas others were treated with the alpha₁-adrenoceptor antagonist prazosin (3 × 10^-7 mol/L), or the alpha₂-adrenoceptor antagonist rauwolscine (10^-7 mol/L). In quiescent rings cooling from 37° C to 24° C had no significant effect. Norepinephrine (10^-8 -10^-5 mol/L) caused concentration-dependent contractions with an EC₂₀ (-log concentration of norepinephrine required to induce contractions 20% of maximal) = 6.97 ± 0.10. The contractions were inhibited by prazosin (EC₂₀ = 5.89 ± 0.17, p < 0.001) and rauwolscine (ED₂₀ = 5.78 ± 0.11, p < 0.001). In control rings cooling potentiated contractions evoked at concentrations of norepinephrine below 10^-6 mol/L and inhibited those at higher concentrations. In rings treated with alpha-antagonists cooling depressed the maximal contractile responses. Contractions to the alpha₁-agonist, phenylephrine (10^-7-10^-4 mol/L), were inhibited by cooling, whereas those to the alpha₂-specific agonist B-HT 920 (10^-7-10^-4 mol/L) showed a pattern similar to that seen with norepinephrine. The data indicate that the human saphenous vein possesses both alpha₁- and alpha₂-adrenoceptors postjunctionally, and that both contribute to contractile responses. Cold augments saphenous vein reactivity to norepinephrine by an apparent increase in the responsiveness of alpha₂-adrenoceptors to agonists. The relationship between temperature and adrenoceptor responsiveness may be of pivotal importance in defining the mechanism of cold-induced vasospasm.