ROLE OF ATRIAL-NATRIURETIC-FACTOR IN IMPAIRED SODIUM-EXCRETION OF NORMOCAPNIC AND HYPERCAPNIC PATIENTS WITH CHRONIC OBSTRUCTIVE LUNG-DISEASE

To investigate the mechanisms of sodium retention in patients with chr onic obstructive lung disease (COLD), we examined the renal and hormon al responses to volume expansion with isotonic saline and to infusion of atrial natriuretic factor (ANF) in 10 hypercapnic (Pa(CO2) 52 +/- 2 mm Hg) and 12 normocapnic patients (Pa(CO2) 39 +/- 1 mm Hg). Sodium e xcreted within 4 h of loading (expressed as % sodium load) was 23.5 +/ - 2.5% (p < 0.05) in normocapnic and 8.5 +/- 1.5% (p < 0.001) in hyper capnic patients, compared with 32.5 +/- 3.0% in 11 age-matched control subjects. Sodium excretion and renal blood flow correlated negatively with arterial P(CO2) and positively with FEV1. Basal plasma ANF conce ntrations were 72 +/- 5 pg/ml in controls, 100 +/- 14 pg/ml in normoca pnic patients, and 230 +/- 52 pg/ml in hypercapnic patients (p < 0.001 ). Plasma renin activity and aldosterone did not differ between groups . In response to volume expansion, plasma ANF increased in both normoc apnic and controls (with a greater increase in normocapnic patients) b ut remained unchanged in hypercapnic patients. Exogenous ANF increased glomerular filtration rate, renal plasma flow, natriuresis, and diure sis in both groups of patients. Patients with COLD have depressed rena l function that appears unrelated to activation of the renin-angiotens in-aldosterone system. An increased secretory response of ANF to volum e expansion may help to maintain volume homeostasis in normocapnic pat ients, while a blunted secretory response of ANF may contribute to sod ium retention in hypercapnic patients.