Diuretic effect of hypoxia, hypocapnia, and hyperpnea in humans: relation to hormones and O-2 chemosensitivity

We studied the contributions of hypoxemia, hypocapnia, and hyperpnea to the acute hypoxic diuretic response (HDR) in humans and evaluated the role of peripheral O-2 chemosensitivity and renal hormones in HDR. Thirteen healthy male subjects (age 19-38 yr) were examined after sodium equilibration (int ake: 120 mmol/day) during 90 min of normoxia (NO), poikilocapnic hypoxia (P H), and isocapnic hypoxia (IH) (days 1-3, random order, double blind), as w ell as normoxic voluntary hyperpnea (HP; day 4), matching ventilation durin g IH. O-2 saturation during PH and IH was kept equal to a mean level measur ed between 30 and 90 min of breathing 12% O-2 in a pretest. Urine flow duri ng PH and IH (1.81 +/- 0.92 and 1.94 +/- 1.03 ml/min, respectively) but not during HP (1.64 +/- 0.96 ml/min) significantly exceeded that during NO (co ntrol, 1.38 +/- 0.71 ml/min). Urine flow increases vs. each test day's base line were significant with PH, IH, and HP. Differences in glomerular filtra tion rate, fractional sodium clearance, urodilatin, systemic blood pressure , or leg venous compliance were excluded as factors of HDR. However, slight increases in plasma and urinary endothelin-1 and epinephrine with PH and I H could play a role. In conclusion, the early HDR in humans is mainly due t o hypoxia and hypocapnia. It occurs without natriuresis and is unrelated to O-2 chemosensitivity (hypoxic ventilatory response).