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The pulmonary arterial pressor response to acute hypoxia is generally attributed to pulmo- nary vasoconstriction (1). Moreover, the dem- onstration that the pulmonary pressor response can occur without the intervention of either the autonomic nervous system (2-4) or known neurohumoral mediators (5, 6) has led to the popular view that the pulmonary vasoconstric- tion is a consequence of local effects of acute hypoxia on the vascular wall (7).
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Bergofsky et al. (1963) studied this question.
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