Plasma Levels of Atrial Natriuretic Factor, Renin Activity, and Aldosterone in Patients with Chronic Obstructive Pulmonary Disease: Response to O2Removal and to Hyperoxia

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Abstract
To examine the interrelations between humoral systems involved in the circulatory and body fluid volume homeostasis of patients with chronic obstructive pulmonary disease (COPD), we measured plasma levels of renin activity (PRA), aldosterone (Aldo), and atrial natriuretic factor (ANF) in 14 patients with stable COPD who used continuous O2 therapy. Hemodynamics, blood gases, and plasma hormone levels were measured (1) while patients received supplemental O2; (2) after 30 min O2 discontinuation; and (3) after a 30-min period of 96% O2 breathing. Plasma immunoreactive ANF concentrations were 196 .+-. 50 pg/ml during O2 breathing and were positively related to transmural pulmonary arterial wedge pressure (tPpaw, r = 0.90, p < 0.001) and to PaCO2 (r = 0.57, p < 0.02). Compared to normal subjects matched for age and sex, patients had higher plasma ANF levels (196 .+-. 52 versus 72 .+-. 6 pg/ml, p < 0.01), similar PRA (2.1 .+-. 0.5 versus 1.3 .+-. 0.3 ng/ml/h, NS), and slightly lower plasma Aldo (98 .+-. 17 versus 156 .+-. 19 pg/ml, p < 0.05). Discontinuation of O2 while decreasing PaO2 from 70 .+-. 3 to 50 .+-. 3 mm Hg resulted in a significant increase in pulmonary arterial pressure (Ppa) from 29 .+-. 2 to 32.5 .+-. 3 mm Hg (p < 0.01) and cardiac index (CI) from 3.6 .+-. 0.1 to 3.9 .+-. 0.1 L/min/m2 (p < 0.01) and a decrease in systemic arterial pressure (Psa) from 96 .+-. 3 to 91 .+-. 2 mm Hg (p < 0.05); transmural cardiac filling pressures and pulmonary vascular resistance (PVR) were unchanged. Despite that plasma ANF tended to increase from 196 .+-. 50 to 253 .+-. 74 pg/ml and Aldo to decrease from 98 .+-. 17 to 76 .+-. 10 pg/ml, there was no significant hormonal variation with O2 removal. Plasma ANF increased in nine patients who differed from the other five patients by a lower PaO2 after O2 discontinuation. Changes in plasma Aldo correlated with changes in arterial pH (r = -0.62, p < 0.02) but not with changes in plasma ANF. Breathing 96% O2 was associated with a rise in Sap and a decrease in Cl, Ppa, and PVR, with no change in Aldo, ANF, and PRA. The results show that in this population of stable patients with COPD, high plasma ANF levels were measured without evidence of simultaneous activation of the reninangiotensin-aldosterone system. Brief variations in the level of oxygenation in these patients did not significantly influence the level of these hormones despite associated hemodynamic changes. Changes in individual plasma Aldo did not appear related to changes in ANF but rather to a hypoxia-induced rise in pH.