Enhanced beta-adrenergic-receptor responsiveness in hypoxic neonatal pulmonary circulation

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Abstract
The influence of alveolar hypoxia on pulmonary vascular adrenergic receptors was studied in conscious newborn lambs. In control animals, pulmonary vessels were directly constricted by epinephrine and norepinephrine, but were unaffected by isoproterenol. Pulmonary resistance (PVR) was also unaffected by propranolol, implying minimal .beta.-receptor activity under normoxic conditions. Hypoxia raised PVR but modified the pulmonary vascular responses to catecholamines: isoproterenol became a dilator, whereas the constrictor effects of epinephrine and norepinephrine were abolished. Although .beta.-blockade did not alter base-line PVR, propranolol increased the constrictor response to hypoxia, implying that hypoxia increases .beta.-adrenergic activity or reactivity in the pulmonary circulation. Consistent with this hypothesis are that in .alpha.-blocked lambs, epinephrine was without local effects during normoxia, but caused vasodilation during hypoxia; the absent constrictor response to epinephrine during hypoxia was fully restored by propranolol; and although .alpha.-blockade blunted the hypoxic constrictor response, the full response was restored when .beta.-blockade was added. The hypoxic constrictor response was partially opposed by increased .beta.-mediated vasodilation. These enhanced .beta.-receptor effects are due, at least in part, to increased .beta.-receptor reactivity of unknown mechanism.