An exaggerated increase in pulmonary arterial systolic pressure (
PAsP) is a highlight of high altitude
pulmonary edema (HAPE). However, the incidence of HAPE at 4559 m was much lower in altitude-naïve individuals with exaggerated pulmonary vasoconstriction (HPV) in normobaric
hypoxia than in known HAPE-susceptibles, indicating that elevated
PAsP alone is insufficient to induce HAPE. A decreased nasal potential difference (
NPD) has been found in HAPE-susceptibles, where, based on animal models,
NPD serves as surrogate of alveolar epithelial ion transport. We hypothesize that those HAPE-resistant individuals with high HPV may be protected by elevated alveolar Na and fluid reabsorption, which might be detected as increased
NPD. To test this hypothesis, we measured
NPD in normoxia of subjects who were phenotyped in previous studies as high altitude tolerant (controls), known HAPE-susceptibles with high HPV (HP+HAPE), as well as individuals with high HPV but without HAPE (HP-no-HAPE) at 4559 m.
NPD and
amiloride-sensitive
NPD were lower in HP+HAPE than in controls, whereas HP-no-HAPE were not different from either group. There were no differences in Cl-transport between groups. Our results show low nasal ion transport in HAPE but higher transport in those individuals with the highest HPV but without HAPE. This indicates that in some individuals with high
PAsP at high altitude high alveolar fluid reabsorption might protect them from HAPE.