High altitude pulmonary oedema (HAPE) is a severe form of altitude illness that develops in travellers on rapid ascent to or physical exertion at altitudes of >2500 m.¹ The disease is characterised by pulmonary hypertension, uneven vasoconstriction, and overperfusion which is thought to cause stress failure of pulmonary capillaries leading to alveolar flooding.¹ Since uneven pulmonary vasoconstriction appears to play an important part in the development of HAPE, the genes involved in maintaining pulmonary vascular tone—for example, angiotensin converting enzyme (ACE) and endothelin-1 (ET-1)—could be possible candidates for HAPE.

Earlier studies showed that the selective pressure of hypobaric hypoxia acted in favour of those alleles of ACE and ET-1 which were beneficial in maintaining a healthy state at high altitude.^2,3 On the other hand, unfavourable alleles are likely to contribute to the susceptibility to HAPE. This hypothesis lends support to an earlier report on the allelic variants of endothelial nitric oxide synthase gene.⁴

We therefore investigated ACE insertion/deletion (I/D) (GenBank accession no X62855) and ET-1 5′-untranslated region (UTR) microsatellite …