Background—Arginine vasopressin (AVP) not only acts directly on blood vessels through V1 receptor stimulation but also may modulate adrenergic-mediated responses in animal experiments in vivo and in vitro. The aim of the present study was to investigate whether AVP can contribute to an abnormal adrenergic constrictor response of human saphenous veins. Methods and Results—Saphenous vein rings were obtained from 32 patients undergoing coronary artery bypass surgery. The vein rings were suspended in organ bath chambers for isometric recording of tension. AVP (331029 mol/L) enhanced the contractions elicited by electrical field stimulation at 1, 2, and 4 Hz (by 80%, 70%, and 60%, respectively) and produced a leftward shift of the concentration-response curve to norepinephrine (half-maximal effective concentration decreased from 6.8731027 to 1.0431027 mol/L; P,.05). The V1 vasopressin receptor antagonist d(CH2)5Tyr(Me)AVP (1026 mol/L) prevented the potentiation evoked by AVP. The selective V1 receptor agonist [Phe,2 Orn8]-vasotocin (331029 mol/L) induced potentiation of electrical stimulation– evoked responses, which was also inhibited in the presence of the V1 receptor antagonist (1026 mol/L). In contrast, the V2 receptor agonist desmopressin (1029 to 1027 mol/L) did not modify neurogenic responses, and the V2 receptor antagonist [d(CH2)5, D-Ile,2 Ile,4 Arg8]-vasopressin (1028 to 1026 mol/L) did not prevent the potentiation induced by AVP. The dihydropyridine calcium antagonist nifedipine (1026 mol/L) did not affect the potentiating effect of AVP. Conclusions—The results suggest that low concentrations of AVP facilitate sympathetic neurotransmission and potentiate constrictor effects of norepinephrine in human saphenous veins. These effects appear to be mediated by V1 receptor stimulation and are independent of calcium entry through dihydropyridine calcium channels. Thus, AVP may contribute to vascular mechanisms involved in acute ischemic syndromes associated with venous grafts, particularly if the sympathetic nervous system is activated. (Circulation. 1998;97:865-870.)