TY - JOUR
T1 - Diuretic effect of acute hypoxia in humans
T2 - Relationship to hypoxic ventilatory responsiveness and renal hormones
AU - Swenson, E. R.
AU - Duncan, T. B.
AU - Goldberg, S. V.
AU - Ramirez, G.
AU - Ahmad, S.
AU - Schoene, R. B.
PY - 1995
Y1 - 1995
N2 - Acute hypoxia causes increased sodium and water excretion. Animal studies suggest that this renal response is largely driven by direct peripheral arterial chemoreceptor stimulation, independent of accompanying changes in ventilation and acid-base status. Whether the diuresis and natriuresis observed in humans made acutely hypoxic are caused by peripheral chemoreceptor stimulation is not known, but, if so, we hypothesized that people with a high ventilatory response to hypoxia (high peripheral chemosensitivity) should have greater diuresis and natriuresis than those with a low ventilatory response to hypoxia. The isocapnic hypoxic ventilatory response (IF/R) of 16 subjects on a fixed sodium intake was measured, as were their urinary volume and sodium and bicarbonate losses during 6 h of breathing air (in a normobaric environmental chamber) and, on the subsequent day, 12% O2. The isocapnic HVR correlated positively with hypoxic diuresis (r = 0.87) and natriuresis (r = 0.76). In contrast, the isocapnic HVR did not correlate with bicarbonate excretion, despite the expected respiratory alkalosis of acute hypoxia. The magnitude of diuresis and natriuresis with hypoxia did not correlate with changes in circulating aldosterone, renin, atrial natriuretic peptide, vasopressin, or a digoxin-like immunoreactive substance. These findings are compatible with a role of the peripheral arterial chemoreceptors in mediating the renal response to hypoxia in humans. The efferent pathway remains unknown.
AB - Acute hypoxia causes increased sodium and water excretion. Animal studies suggest that this renal response is largely driven by direct peripheral arterial chemoreceptor stimulation, independent of accompanying changes in ventilation and acid-base status. Whether the diuresis and natriuresis observed in humans made acutely hypoxic are caused by peripheral chemoreceptor stimulation is not known, but, if so, we hypothesized that people with a high ventilatory response to hypoxia (high peripheral chemosensitivity) should have greater diuresis and natriuresis than those with a low ventilatory response to hypoxia. The isocapnic hypoxic ventilatory response (IF/R) of 16 subjects on a fixed sodium intake was measured, as were their urinary volume and sodium and bicarbonate losses during 6 h of breathing air (in a normobaric environmental chamber) and, on the subsequent day, 12% O2. The isocapnic HVR correlated positively with hypoxic diuresis (r = 0.87) and natriuresis (r = 0.76). In contrast, the isocapnic HVR did not correlate with bicarbonate excretion, despite the expected respiratory alkalosis of acute hypoxia. The magnitude of diuresis and natriuresis with hypoxia did not correlate with changes in circulating aldosterone, renin, atrial natriuretic peptide, vasopressin, or a digoxin-like immunoreactive substance. These findings are compatible with a role of the peripheral arterial chemoreceptors in mediating the renal response to hypoxia in humans. The efferent pathway remains unknown.
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U2 - 10.1152/jappl.1995.78.2.377
DO - 10.1152/jappl.1995.78.2.377
M3 - Article
C2 - 7759405
AN - SCOPUS:0028878241
VL - 78
SP - 377
EP - 383
JO - Journal of Applied Physiology
JF - Journal of Applied Physiology
SN - 8750-7587
IS - 2
ER -