Acute
hypoxia causes
hyperventilation and
respiratory alkalosis, often combined with increased diuresis and
sodium,
potassium, and
bicarbonate excretion. With a low
sodium intake, the excretion of the
anion bicarbonate may be limited by the lower excretion rate of the
cation sodium through activated
sodium-retaining mechanisms. This study investigates whether the short-term renal compensation of
hypoxia-induced
respiratory alkalosis is impaired by a low
sodium intake. Nine conscious, tracheotomized dogs were studied twice either on a low-
sodium (LS = 0.5 mmol
sodium x kg body wt-1 x day-1) or high-
sodium (HS = 7.5 mmol
sodium x kg body wt-1 x day-1) diet. The dogs breathed spontaneously via a
ventilator circuit during the experiments: first hour, normoxia (inspiratory
oxygen fraction = 0.21); second to fourth hour,
hypoxia (inspiratory
oxygen fraction = 0.1). During
hypoxia (arterial PO2 34.4 +/- 2.1 Torr), plasma pH increased from 7.37 +/- 0.01 to 7.48 +/- 0.01 (P < 0.05) because of
hyperventilation (arterial PCO2 25.6 +/- 2.4 Torr). Urinary pH and urinary
bicarbonate excretion increased irrespective of the
sodium intake.
Sodium excretion increased more during HS than during LS, whereas the increase in
potassium excretion was comparable in both groups. Thus the quick onset of
bicarbonate excretion within the first hour of
hypoxia-induced
respiratory alkalosis was not impaired by a low
sodium intake. The increased
sodium excretion during
hypoxia seems to be combined with a decrease in plasma
aldosterone and
angiotensin II in LS as well as in HS dogs. Other factors, e.g., increased mean arterial blood pressure, minute ventilation, and renal blood flow, may have contributed.