THE CATECHOLAMINES IN THE PULMONARY ARTERIAL PRESSOR RESPONSE TO ACUTE HYPOXIA*

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Abstract
Acute hypoxia induced in normal man by the inhalation of ll[degree]/o oxygen was not associated with an increase in levels of circulating epinephrine (E) or norepine-phrine (NE). During ambient air breathing, the circulating level of NE had to be increased at least thirteen times above control levels in order to duplicate the pulmonary arterial pressor response to acute hypoxia. This infusion of NE elicited pulmonary arterial hypertension by a mechanism different from that of acute hypoxia. An increase in the level of circulating NE by infusion during acute hypoxia did not exaggerate the pulmonary pressor response. Supplemental observation on dogs revealed that depletion of pulmonary vascular nerve endings of NE by reserpine did not prevent the pulmonary arterial pressor response to acute hypoxia. The study provides no evidence for a role of catecholamines in the pulmonary arterial pressor response to acute hypoxia in normal man.