Abstract

We have used in vitro preparations of human penile dorsal artery and deep dorsal vein from 20 multiorgan donors to investigate whether subpressor concentrations of vasopressin facilitate noradrenergic transmission in penile blood vessels. Vasopressin constricted penile dorsal arteries (pD₂, 9.38 ± 0.18) and deep dorsal veins (pD₂, 9.40 ± 0.14) by activating V₁ receptors. Vasopressin (10⁻¹¹ and 3 × 10⁻¹¹ 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 V₁ receptor antagonist d(CH₂)₅Tyr(Me)AVP (3 × 10⁻⁹-10⁻⁷ M) induced concentration-dependent inhibitions of potentiation caused by vasopressin. In contrast, the V₂ receptor antagonist [d(CH₂)₅,d-Ile², Ile⁴,Arg⁸]-vasopressin (10⁻⁸-10⁻⁷ M) did not prevent the potentiation induced by vasopressin. The results demonstrate that vasopressin exerts powerful constrictor action in human penile arteries and veins by direct stimulation of V₁receptors. In addition, vasopressin strongly potentiates the contractions to norepinephrine and stimulation of perivascular adrenergic nerves. Consequently, the direct contractile effects of vasopressin together with its amplifying effects on adrenergic-mediated constriction should be taken into consideration in the overall regulation of penile erection and in those states characterized by increased plasma vasopressin levels.