Our objectives were to investigate the extent to which both exogenously administered and endogenously released arginine vasopressin (AVP) exert a direct, vasoactive influence on the pulmonary circulation of conscious dogs. 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 (IVC) to reduce Q̇. In intact dogs, AVP infusion (7.6 ng·kg-1·min-1 iv) increased (P < 0.01) plasma AVP from 2.3 ± 0.4 to 280 ± 23 pg/ml, and increased (P < 0.01) the pulmonary vascular pressure gradient (pulmonary arterial pressure minus pulmonary capillary wedge pressure, PAP - PCWP) over the entire range of Q̇ studied. Following administration of autonomic nervous system antagonists and a converting-enzyme inhibitor, exogenous AVP again increased (P < 0.01) PAP - PCWP over the entire range of Q̇. Generation of P/Q̇ plots via IVC constriction resulted in systemic hypotension (58 ± 4 mmHg) and a concomitant increase (P < 0.01) in endogenous AVP release from 2.1 ± 0.2 to 109 ± 22 pg/ml. Following administration of the specific AVP receptor antagonist [d(CH2)5]AVP (10 μg/kg iv), systemic arterial pressure, but not PAP - PCWP, was decreased to significantly lower levels as Q̇ was reduced during IBV constriction. A similar response was observed in dogs pretreated with the neurohumoral blockers. Thus exogenous administration of AVP results in active, non-flow-dependent pulmonary vasoconstriction. The effect is not dependent on reflex activation of the autonomic nervous system or on the increased production of angiotensin II. In contrast, AVP block had no effect on P/Q̇ when AVP was released from endogenous sources during systemic hypotension.
|Original language||English (US)|
|Journal||American Journal of Physiology - Heart and Circulatory Physiology|
|State||Published - Dec 1 1986|
ASJC Scopus subject areas
- Cardiology and Cardiovascular Medicine
- Physiology (medical)