ROLE OF VASOPRESSIN ON ADRENERGIC NEUROTRANSMISSION IN HUMAN PENILE BLOOD-VESSELS

We have used in vitro preparations of human penile dorsal artery and d eep dorsal vein from 20 multiorgan donors to investigate whether subpr essor concentrations of vasopressin facilitate noradrenergic transmiss ion in penile blood vessels. Vasopressin constricted penile dorsal art eries (pD(2),, 9.38 +/- 0.18) and deep dorsal veins (pD(2),, 9.40 +/- 0.14) by activating V-1, receptors. Vasopressin (10(-11) and 3 x 10(-1 1) M) caused concentration-dependent potentiation of the contractions elicited by electrical stimulation (15 V, 0.5-2 Hz, 0.2 msec duration for 15 sec) and produced leftward shifts of the concentration-response curve for norepinephrine. The V-1 receptor antagonist d(CH2)(5)Tyr(Me )AVP (3 x 10(-9)-10(-7) M) induced concentration-dependent inhibitions of potentiation caused by vasopressin. In contrast, the V-2, receptor antagonist [d(CH2)5,D-IIe(2),IIe(4),Arg(8)]-vasopressin (10(-8)-10(-7 ) M) did not prevent the potentiation induced by vasopressin. The resu lts demonstrate that vasopressin exerts powerful constrictor action in human penile arteries and veins by direct stimulation of V-1, recepto rs. in addition, vasopressin strongly potentiates the contractions to norepinephrine and stimulation of perivascular adrenergic nerves. Cons equently, the direct contractile effects of vasopressin together with its amplifying effects on adrenergic-mediated constriction should be t aken into consideration in the overall regulation of penile erection a nd in those states characterized by increased plasma vasopressin level s.