TY - JOUR
T1 - Pulmonary vascular responses to angiotensin II and captopril in conscious dogs
AU - Goll, H. M.
AU - Nyhan, D. P.
AU - Geller, H. S.
AU - Murray, P. A.
PY - 1986
Y1 - 1986
N2 - Our objectives were to investigate the extent to which angiotensin II (ANG II) and converting-enzyme inhibition (CEI) 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 to reduce Q̇. The effects of ANG II infusion (60 ng·kg-1·min-1, iv) and CEI with captopril (1 mg/kg plus 1 mg·kg-1·h-1, iv) on pulmonary vascular P/Q̇ plots were assessed first with the conscious dogs intact and again after combined administration of pharmacological antagonists to block sympathetic α- and β-adrenergic, cholinergic, and arginine vasopressin receptors. In intact dogs, ANG II increased (P < 0.01) the pulmonary vascular pressure gradient (pulmonary arterial pressure-pulmonary capillary wedge pressure, PAP-PCWP) over the entire range of Q̇ studied (60-120 ml·min-1·kg-1). Conversely, CEI decreased (P < 0.05) PAP-PCWP at each level of Q̇. After administration of the autonomic nervous system and arginine vasopressin receptor antagonists, ANG II again increased (P < 0.01) and CEI decreased (P < 0.01) PAP-PCWP over the entire range of Q̇ studied. Thus exogenous administration of ANG II results in active, nonflow-dependent constriction of the pulmonary circulation, and this effect is not dependent on the autonomic nervous system or increased circulating levels of arginine vasopressin. Moreover, the active, nonflow-dependent vasodilation observed during CEI before and after neurohumoral block supports the concept that endogenous ANG II exerts a vasoconstrictor influence on the pulmonary circulation over a broad range of cardiac index in conscious dogs.
AB - Our objectives were to investigate the extent to which angiotensin II (ANG II) and converting-enzyme inhibition (CEI) 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 to reduce Q̇. The effects of ANG II infusion (60 ng·kg-1·min-1, iv) and CEI with captopril (1 mg/kg plus 1 mg·kg-1·h-1, iv) on pulmonary vascular P/Q̇ plots were assessed first with the conscious dogs intact and again after combined administration of pharmacological antagonists to block sympathetic α- and β-adrenergic, cholinergic, and arginine vasopressin receptors. In intact dogs, ANG II increased (P < 0.01) the pulmonary vascular pressure gradient (pulmonary arterial pressure-pulmonary capillary wedge pressure, PAP-PCWP) over the entire range of Q̇ studied (60-120 ml·min-1·kg-1). Conversely, CEI decreased (P < 0.05) PAP-PCWP at each level of Q̇. After administration of the autonomic nervous system and arginine vasopressin receptor antagonists, ANG II again increased (P < 0.01) and CEI decreased (P < 0.01) PAP-PCWP over the entire range of Q̇ studied. Thus exogenous administration of ANG II results in active, nonflow-dependent constriction of the pulmonary circulation, and this effect is not dependent on the autonomic nervous system or increased circulating levels of arginine vasopressin. Moreover, the active, nonflow-dependent vasodilation observed during CEI before and after neurohumoral block supports the concept that endogenous ANG II exerts a vasoconstrictor influence on the pulmonary circulation over a broad range of cardiac index in conscious dogs.
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U2 - 10.1152/jappl.1986.61.4.1552
DO - 10.1152/jappl.1986.61.4.1552
M3 - Article
C2 - 3096940
AN - SCOPUS:0023037265
VL - 61
SP - 1552
EP - 1559
JO - Journal of Applied Physiology
JF - Journal of Applied Physiology
SN - 0161-7567
IS - 4
ER -