ABSTRACT
Hypoxic pulmonary vasoconstriction (HPV) is a highly specialized response of the pulmonary circulation to hypoxic challenge. It manifests itself as a pressor response in vivo or in perfused lung and as a contraction in isolated small pulmonary arteries and pulmonary artery smooth muscle cells (PASMCs). At least a component of the mechanisms underlying HPV must reside in the PASMC itself, although there is considerable evidence that several exogenous factors derived from the endothelium play a facilitatory, permissive, and=or modulatory role for the full development of HPV. In particular, an intact endothelium appears to be essential for the development of sustained (> 20min) HPV, via a Rho-kinase-mediated increase in Ca2þ sensitivity of the underlying smooth muscle (see Ref. 1). Nevertheless, it is universally accepted that a rise in PASMC intracellular Ca2þ concentration ([Ca2þ]i) is critical for HPV, and there is general consensus that this involves Ca2þ entry via one or several types of ion channels, although it has been suggested that release of Ca2þ from the sarcoplasmic reticulum alone may be sufficient (2). This chapter briefly reviews the potential role of the various types of ion channels that have been or could be implicated in the rise of intracellular [Ca2þ] during HPV.
