ARGININE-VASOPRESSIN ENHANCES SYMPATHETIC CONSTRICTION THROUGH THE V-1 VASOPRESSIN RECEPTOR IN HUMAN SAPHENOUS-VEIN

Background-Arginine vasopressin (AVP) not only acts directly on blood vessels through V-1 receptor stimulation but also may modulate adrener gic-mediated responses in animal experiments in vivo and in vitro. The aim of the present study was to investigate whether AVP can contribut e to an abnormal adrenergic constrictor response of human saphenous ve ins. Methods and Results-Saphenous vein rings were obtained from 32 pa tients undergoing coronary artery bypass surgery. The vein rings were suspended in organ bath chambers for isometric recording of tension. A VP (3X10(-9) mol/L) enhanced the contractions elicited by electrical f ield 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 .87X10(-7) to 1.04X10(-7) mol/L; P<.05). The V-1 vasopressin receptor antagonist d(CH2)(5)Tyr(Me)AVP (10(-6) mol/L) prevented the potentiati on evoked by AVP. The selective V-1 receptor agonist [Phe,(2) Orn(8)]- vasotocin (3X10(-9) mol/L) induced potentiation of electrical stimulat ion-evoked responses, which was also inhibited in the presence of the V-1 receptor antagonist (10(-6) mol/L). In contrast, the V-2 receptor agonist desmopressin (10(-9) to 10(-7) mol/L) did not modify neurogeni c responses, and the V-2 receptor antagonist [d(CH2)(5), D-Ile,(2) Ile ,(4) Arg(8)]-vasopressin (10(-8) to 10(-6) mol/L) did not prevent the potentiation induced by AVP. The dihydropyridine-calcium antagonist ni fedipine (10(-6) mol/L) did not affect the potentiating effect of AVP. Conclusions-The results suggest that low concentrations of AVP facili tate sympathetic neurotransmission and potentiate constrictor effects of norepinephrine in human saphenous veins. These effects appear to be mediated by V-1 receptor stimulation and are independent of calcium e ntry through dihydropyridine calcium channels. Thus, AVP may contribut e to vascular mechanisms involved in acute ischemic syndromes associat ed with venous grafts, particularly if the sympathetic nervous system is activated.