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Lung angiotensin converting enzyme activity in chronically hypoxic rats.
Thorax
|August 1, 1985
Summary
Reduced lung angiotensin converting enzyme (ACE) activity during chronic hypoxia is linked to pulmonary hypertension, not hypoxia itself. Recovery normalized both ACE activity and blood pressure.
Area of Science:
- Physiology
- Cardiovascular Research
- Respiratory Medicine
Background:
- Chronic hypoxia is known to reduce lung angiotensin converting enzyme (ACE) activity.
- The relationship between reduced ACE activity and the development of pulmonary hypertension in hypoxia is not fully understood.
Purpose of the Study:
- To investigate whether reduced lung ACE activity in chronic hypoxia is a cause or consequence of pulmonary hypertension.
- To differentiate the effects of hypoxia per se from the hemodynamic factors associated with pulmonary hypertension on lung ACE activity.
Main Methods:
- Rats were exposed to hypobaric hypoxia (380 mm Hg) for 2 to 24 days.
- Measurements included right ventricular mean systolic pressure (Prvs) and lung tissue ACE activity.
- Recovery groups were monitored for up to 153 days after 24 days of hypoxia.
Main Results:
- After 2 days of hypoxia, Prvs and ACE activity did not differ significantly from controls.
- 4 to 24 days of hypoxia led to increased Prvs and decreased lung ACE activity.
- During recovery, ACE activity and Prvs returned to normal levels by 15 and 56 days, respectively.
Conclusions:
- Reduced lung ACE activity in chronic hypoxia appears to be associated with the hemodynamic changes of pulmonary hypertension.
- The findings suggest that decreased ACE activity is a consequence, rather than a primary cause, of hypoxia-induced pulmonary hypertension.