Abstract
Abstract
Rats were exposed to high-altitude (5500 m) hypoxia for 2 weeks. On examination 1-3 days after return to sea level and compared with control rats, they exhibited pulmonary hypertension, reduced angiotensin-converting enzyme activity, greater vascular responsiveness to angiotensin II (AII), and resistance to blockade of AII pulmonary pressor responses by the AII antagonist, saralasin.
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