Low sodium intake does not impair short-term renal compensation of hypoxia-induced respiratory alkalosis in conscious dogs

Acute hypoxia causes hyperventilation and respiratory alkalosis, often combined with increased diuresis, sodium-, potassiumand bicarbonate excretion. On 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 hypoxiainduced respiratory alkalosis is impaired by a low sodium intake. Nine conscious, tracheotomized dogs were studied twice either on a low sodium diet (LS = 0.5 mmol sodium per kg body weight (body wt) per day), or on a high sodium diet (HS = 7.5 mmol sodium·kg body wt·day). The dogs were breathing spontaneously via a ventilator circuit during the experiments: first hour, normoxia (FiO2 = 0.21, inspiratory oxygen fraction); second to fourth hour, hypoxia (FiO2 = 0.1). During hypoxia (PaO2 34.4±2.1 mm Hg), plasma pH increased from 7.37±0.01 to 7.48±0.01 (P<0.05) due to hyperventilation (PaCO2 25.6±2.4 mm Hg). 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. In conclusion, 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 MAP, minute ventilation and renal blood flow may have contributed.