Hypoxic pulmonary vasoconstriction and their roles in pulmonary hypertension: new findings for an old problem

Mechanisms that have been implicated in the hypoxia-induced elevation of [Ca2+]i, and their potential signalling pathways. Note that some mechanisms are probably only applicable to one phase of HPV (see text). Not shown for clarity: possibility of functionally different types of SOC and Ca2+ store. Note that Na+ entry via NSCC would also contribute to depolarisation. The boxes highlight studies from the last 2 years that address that pathway or channel. †: action of Mg2+ and ATP on KV channels depends on membrane potential (see text). DAG, diacylglycerol; cADPR, cyclic ADP ribose; depol, depolarization; KV, voltage-gated K+ channels; L-type, voltage-gated Ca2+ channels; NCX, Na+-Ca2+ exchanger; RyR, ryanodine receptors; SOC, store operated channels.

Publication

Mechanisms of hypoxic pulmonary vasoconstriction and their roles in pulmonary hypertension: new findings for an old problem. () Jeremy P.T. Ward, et al. Curr Opin Pharmacol. ;9(3):287-296. Figure: F2. All organisms Mus musculus Homo sapiens Rattus norvegicus Canis lupus familiaris Oryctolagus cuniculus Drosophila melanogaster

Disease mentions