Adrenergic mechanisms and the pulmonary vascular response to respiratory acidosis.

The role of sympathetic mechanisms in mediating the pulmonary vasoconstrictor response to respiratory acidosis was studied in intact dogs. Arterial oxygen tension and ventilation were maintained at resting levels and the response was studied during a constant level of alpha- and beta-adrenergic blockade. There were significant increases in the pulmonary vascular resistance (PVR) and pulmonary perfusion pressure and no change in pulmonary blood flow (Q) when the dogs breathed 5% CO2 for 10 min. The alpha-adrenergic blocking agent, phenoxybenzamine, did not significantly alter the pulmonary vascular response, while the beta-adrenergic blocking agent, propranolol, enhanced the response. Phenoxybenzamine significantly reduced the resting pulmonary perfusion pressure from control values, while propranolol did not alter it. Both propranolol and phenoxybenzamine produced comparable decreases in the resting Q from control values. The resting PVR increased to a greater extent with propranolol than with phenoxybenzamine. These results indicate that adrenergic mechanisms do not play a role in mediating rise in PVR induced by respiratory acidosis. The finding that the pulmonary vasoconstrictor response to respiratory acidosis is enhanced during beta-adrenergic blockade suggests that vasoconstrictor alpha-receptors may be unmasked during beta-adrenergic blockade. Finally, the studies suggest that both alpha- and beta-receptors contribute to maintaining the resting PVR.