AJP - Heart and Circulatory Physiology, Vol 253, Issue 3 493-H499, Copyright © 1987 by American Physiological Society
AVP-induced pulmonary vasodilation during specific V1 receptor block in conscious dogs
D. P. Nyhan, P. W. Clougherty and P. A. Murray
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 beta-adrenergic or cholinergic receptor activation or by
cyclooxygenase pathway activation. Multipoint pulmonary vascular
pressure-cardiac index (P/Q) plots were constructed during normoxia in
conscious dogs by stepwise constriction of the thoracic inferior vena cava
to reduce Q. In dogs pretreated with a specific V1 receptor antagonist
[d(CH2)5 AVP, 10 micrograms/kg iv], AVP infusion (7.6 ng.kg-1 X min-1 iv)
increased (P less than 0.01) Q from 139 +/- 6 to 175 +/- 8 ml.min-1 X kg-1,
and decreased (P less than 0.01) the pulmonary vascular pressure gradient
(pulmonary arterial pressure-pulmonary capillary wedge pressure: PAP-PCWP)
over the entire range of Q studied (140 to 80 ml.min-1 X kg-1). This
pulmonary vasodilator response to AVP during V1 block was also observed
following sympathetic beta-adrenergic block alone, following combined
sympathetic beta-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 beta-adrenergic or cholinergic
receptors or by metabolites of the cyclooxygenase pathway over a broad
range of Q.
