EFFECTS OF ANGIOTENSIN-CONVERTING ENZYME-INHIBITION ON SODIUM-EXCRETION IN PATIENTS WITH HYPOXEMIC CHRONIC OBSTRUCTIVE PULMONARY-DISEASE

Background - Some patients with hypoxaemic chronic obstructive pulmona ry disease (COPD) develop cor pulmonale with sodium and water retentio n. The sodium retention has been explained as a result of increased pl asma levels of aldosterone. If this was true angiotensin converting en zyme (ACE) inhibition would be expected to lower plasma levels of aldo sterone and improve the renal excretion of sodium. Methods - Six patie nts with stable hypoxaemic COPD (Pao(2) <8.0 kPa) and a history of an oedematous exacerbation received an intravenous hypertonic saline load (6 ml/kg body weight of 2.7% saline over one hour) before and while t aking 4 mg/day perindopril, an ACE inhibitor, for one month. Aldostero ne, antidiuretic hormone (ADH), plasma and urine electrolyte levels, o smolality, and volume were measured over four hours. The repeatability of the saline load test was assessed in six patients with a similar s everity of hypoxaemic COPD. For comparison the saline load test was al so performed in six patients with mild COPD. Results - The hypertonic saline load test results were repeatable. Perindopril reduced the mean (SD) plasma level of aldosterone from 142 (88) pg/ml to 54 (24) pg/ml at 0 minutes before the saline infusion, and from 64 (35) pg/ml to 30 (17) pg/ml after the infusion without improving the urinary volume or sodium excretion. Before starting treatment with perindopril 43.7 (6. 9) mmol (20%) of the sodium load was excreted compared with 49.6 (7.9) mmol (22% of load) when taking perindopril. Patients with mild COPD e xcreted more sodium (77.6 (21.4) mmol (38.7% of load)) despite having similar plasma aldosterone levels to those in the patients receiving p erindopril. Conclusions - Patients with stable hypoxaemic COPD have an impaired ability to excrete sodium which is not improved by the admin istration of an ACE inhibitor. ACE inhibition lowered the plasma level of aldosterone without improving sodium excretion. This suggests that the inability of patients with hypoxaemic COPD to excrete sodium is n ot caused by their increased plasma levels of aldosterone.