AVP-induced pulmonary vasodilation during specific V₁ receptor block in conscious dogs

Our objectives were 1) to determine whether exogenously administered arginine vasopressin (AVP) can exert a vasoactive influence on the pulmonary circulation of conscious dogs during specific vasopressinergic-1 (V₁) receptor block, and 2) to assess the extent to which the pulmonary vascular response to AVP during V₁ receptor block is mediated by either sympathetic β-adrenergic or cholinergic receptor activation or by cyclooxygenase pathway activation. Multipoint pulmonary vascular pressure-cardiac index (P/Q̇) plots were constructed during normoxia in conscious dogs by stepwise constriction of the thoracic inferior vena cava to reduce Q̇. In dogs pretreated with a specific V₁ receptor antagonist [d(CH₂)₅AVP, 10 μg/kg iv], AVP infusion (7.6 ng·kg^-1·min-¹ iv) increased (P < 0.01) Q̇ from 139 ± 6 to 175 ± 8 ml·min^-1·kg^-1, and decreased (P < 0.01) the pulmonary vascular pressure gradient (pulmonary arterial pressure-pulmonary capillary wedge pressure: PAP-PCWP) over the entire range of Q̇ studied (140 to 80 ml·min^-1·kg^-1). This pulmonary vasodilator response to AVP during V₁ block was also observed following sympathetic β-adrenergic block alone, following combined sympathetic β-adrenergic and cholinergic block, and following cyclooxygenase pathway inhibition. Thus exogenous administration of AVP during specific V₁ receptor block results in active, nonflow-dependent pulmonary vasodilation. This pulmonary vasodilator response is not mediated by reflex activation of sympathetic β-adrenergic or cholinergic receptors or by metabolites of the cyclooxygenase pathway over a broad range of Q̇.