Journal
BRITISH JOURNAL OF PHARMACOLOGY
Volume 178, Issue 1, Pages 121-131Publisher
WILEY
DOI: 10.1111/bph.15144
Keywords
genetics; high-altitude; hypoxia-inducible factor; hypoxiainducible factor prolyl hydroxylase 2; oxygen sensing; pulmonary vasoconstriction; vascular remodelling
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Funding
- British Heart Foundation [PG/18/2/33446, PG/12/61/29818] Funding Source: Medline
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Exposure to global alveolar hypoxia leads to increased pulmonary artery pressure in adult mammals, which is seen as a maladaptive response requiring additional workload on the right ventricle. Understanding the mechanisms behind this elevated pressure is crucial for pulmonary vascular homeostasis. Researchers aim to identify key molecules in the vascular response to hypoxia through genetic and phenotypic studies in highlanders.
An increase in pulmonary artery pressure is a common observation in adult mammals exposed to global alveolar hypoxia. It is considered a maladaptive response that places an increased workload on the right ventricle. The mechanisms initiating and maintaining the elevated pressure are of considerable interest in understanding pulmonary vascular homeostasis. There is an expectation that identifying the key molecules in the integrated vascular response to hypoxia will inform potential drug targets. One strategy is to take advantage of experiments of nature, specifically, to understand the genetic basis for the inter-individual variation in the pulmonary vascular response to acute and chronic hypoxia. To date, detailed phenotyping of highlanders has focused on haematocrit and oxygen saturation rather than cardiovascular phenotypes. This review explores what we can learn from those studies with respect to the pulmonary circulation.
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