From the Department of Physiology (P.M., A.A., J.M.V., M.A., S.L.) and
the Department of Surgery (J.B.M.-L., E.O.), University of Valencia (Spain).
Correspondence to S. Lluch, MD, Department of Physiology, Facultad de Medicina y Odontología, Avda Blasco Ibáñez 17, 46010 Valencia, Spain. E-mail medinap{at}post.uv.es
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 (3x10-9 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
6.87x10-7 to 1.04x10-7 mol/L;
P<.05). The V1 vasopressin receptor
antagonist d(CH2)5Tyr(Me)AVP
(10-6 mol/L) prevented the potentiation evoked by AVP. The
selective V1 receptor agonist [Phe,2
Orn8]-vasotocin (3x10-9 mol/L) induced
potentiation of electrical stimulation–evoked responses, which was
also inhibited in the presence of the V1 receptor
antagonist (10-6 mol/L). In contrast, the
V2 receptor agonist desmopressin (10-9 to
10-7 mol/L) did not modify neurogenic responses, and the
V2 receptor antagonist
[d(CH2)5, D-Ile,2
Ile,4 Arg8]-vasopressin (10-8 to
10-6 mol/L) did not prevent the potentiation induced by
AVP. The dihydropyridine calcium
antagonist nifedipine (10-6 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.
© 1998 American Heart Association, Inc.
Clinical Investigation and Reports
Arginine Vasopressin Enhances Sympathetic Constriction Through the V1 Vasopressin Receptor in Human Saphenous Vein
Key Words: veins • arginine vasopressin • electrical stimulation • norepinephrine
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