SEROTONIN-INDUCED CORTISOL RELEASE IN CPAP-TREATED OBSTRUCTIVE SLEEP-APNEA PATIENTS

Previously, we demonstrated elevated cortisol production/release in re sponse to the administration of the serotonin precursor, L-5-hydroxytr yptophan (L-5-HTP) in untreated patients with obstructive sleep apnea (OSA). We hypothesized that if this elevated cortisol response to L-5- HTP was related to OSA, this finding would not be present in OSA patie nts treated with nasal continuous positive airway pressure (nCPAP). El even OSA patients treated for at least 1 month with nCPAP were studied . On two different days, we measured blood cortisol level every 15 min for 4 h following the ingestion of L-5-HTP, 0.4 mg/kg, or placebo, bo th given with carbidopa, a peripheral tryptophan decarboxylase inhibit or, used to prevent peripheral L-5-HTP metabolism before brain absorpt ion. For a given subject, the cortisol response was calculated as the difference between the area under the curve of the L-5-HTP and placebo responses. In the nCPAP-treated OSA patients, this net cortisol respo nse, 577+/-240 min .mu g/dL, was less than the value found in the prev iously studied untreated OSA group, 1,188+/-227 min .mu g/dL (p<0.05) and not different from the previously studied nonapneic control group, 469+/-154 min mu g/dL From these results, we speculate that nCPAP tre atment reverses the elevated cortisol response to serotonergic stimula tion seen in untreated OSA patients.