Atrial natriuretic peptide levels and plasma volume contraction in acute alveolar hypoxia

Abstract

Albert, T. S. E., V. L. Tucker, and E. M. Renkin.Atrial natriuretic peptide levels and plasma volume contraction in acute alveolar hypoxia. J. Appl. Physiol. 82(1): 102–110, 1997.—Arterial oxygen tensions ([Formula: see text]), atrial natriuretic peptide (ANP) concentrations, and circulating plasma volumes (PV) were measured in anesthetized rats ventilated with room air or 15, 10, or 8% O2( n = 5–7). After 10 min of ventilation, [Formula: see text] values were 80 ± 3, 46 ± 1, 32 ± 1, and 35 ± 1 Torr and plasma immunoreactive ANP (irANP) levels were 211 ± 29, 229 ± 28, 911 ± 205, and 4,374 ± 961 pg/ml, respectively. At[Formula: see text] ≤40 Torr, irANP responses were more closely related to inspired O2( P = 0.014) than to[Formula: see text] ( P= 0.168). PV was 36.3 ± 0.5 μl/g in controls but 8.5 and 9.9% lower ( P ≤ 0.05) for 10 and 8% O2, respectively. Proportional increases in hematocrit were observed in animals with reduced PV; however, plasma protein concentrations were not different from control. Between 10 and 50 min of hypoxia, small increases (+40%) in irANP occurred in 15% O2; however, there was no further change in PV, hematocrit, plasma protein, or irANP levels in the lower O2groups. Urine output tended to fall during hypoxia but was not significantly different among groups. These findings are compatible with a role for ANP in mediating PV contraction during acute alveolar hypoxia.