We have studied serum and lung tissue angiotensin converting enzyme (ACE) activity in female Wistar rats with pulmonary hypertension induced by two different methods. Chronic pulmonary hypertension was produced in one group of 10 rats (CH) by confinement in a hypobaric chamber (380 mmHg) for three weeks, and in another group of 10 rats (M) by a single subcutaneous injection of monocrotaline (60 mg/kg body weight). In these two groups of test rats and in 20 untreated controls (C), we evaluated right ventricular mean systolic blood pressure (Prvs mmHg), right ventricular hypertrophy, and serum ACE (n mol/ml/min). In pancreas, adrenal, liver, and kidney.3 However, it has been calculated that most of the ACE activity in the body occurs in the lungs4 where the enzyme has been localised on the luminal surface of pulmonary endothelial cells in relation to the plasma membrane.5 It has been shown that the pulmonary conversion of angiotensin I to angiotensin II is a function of the vascular surface area and the transit time of blood through the lung.6 Accordingly, it might be expected that diffuse lung disease and pulmonary hypertension in particular would be associated with alterations of lung ACE activity. However, although there have been a few studies of lung ACE activity in acute hypoxia,7 8 chronic hypoxia,9 and acute lung injury,10 11 there has been only one study specifically related to pulmonary hypertension.'2The purpose of this paper is to describe the effect of pulmonary hypertension on lung ACE activity. We induced chronic pulmonary hypertension in one 198 on 8 May 2018 by guest. Protected by copyright.

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