Blunted hypoxic vasoconstriction in lungs from short-term high-altitude rats

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Abstract
Blood-perfused lungs from rats kept at low altitude (1520 m) or exposed for 40 h to simulated high altitude (4270 m) were studied to see if hours of continuous hypoxia caused a selective blunting of the mechanism of hypoxic pulmonary vasoconstriction. High altitude lungs had blunted pressor responses to acute airway hypoxia and to intraarterial KCN and 2,4-dinitrophenol. Hyporeactivity to acute hypoxia could not be attributed to hypocapnia at high altitude but might have been due partly to anorexia. The blunted hypoxic pressor response was not reversed by blockade of histamine-induced vasodilation with chlorpheniramine or by inhibition of prostaglandin synthesis with meclofenamate. Inhibitors of metabolism, 2-deoxyglucose and KCN, increased responsiveness to airway hypoxia in low and high altitude lungs, but did not eliminate the blunted response in high altitude lungs. High altitude lungs had blunted pressor responses to intra-arterial KCl and angiotensin II, and main pulmonary arteries from high altitude rats had blunted contractile responses to the same agonists. Apparently the blunted hypoxic pressor response was associated with a nonspecific decrease in reactivity of the vascular smooth muscle, i.e., the effector of the hypoxic mechanism, rather than with a selective abnormality of the unidentified O2 sensor or precess of tranduction between sensor and effector. The decreased reactivity of the vascular smooth muscle might have been related to a change in its Ca metabolism.