Hypoxia contracts the pulmonary vein but the underlying cellular effectors remain unclear. Utilizing contractile studies and whole-cell patch-clamp electrophysiology, we report for the first time a hypoxia-sensitive K(+) current in porcine pulmonary vein smooth muscle cells (PVSMC). Hypoxia induced a transient contractile response that was 41±7% of the control response (80 mM KCl). This contraction required extracellular Ca(2+) and was sensitive

Small pulmonary arteries (SPA) and veins contract when alveolar pO2 is low. Hypoxic pulmonary vasoconstriction (HPV) is known to release Ca2+ from the SR in SPA. Hypoxia-induced SR Ca2+ release activates ClCa. Agonist-induced contraction in SPA increases when [Cl-]0 is reduced. However, the effects of altering Cl- flux on HPV in the pulmonary vein are not known. Here we show how changes in extracellular Cl- differentially affect SPA and venular contraction

In the pulmonary artery (PA), hypoxia releases Ca2+ from the SR (Dipp et al. 2001) and during hypoxia, Ca2+ released from the SR may activate the Ca2+-activated Cl- channel (ClCa) in the plasma membrane (Wang et al. 1997). Decreasing [Cl-]o can increase agonist-induced contraction in the PA (Lamb & Barna, 1998). Here we report the effects of decreasing [Cl-]o on the hypoxic pulmonary vasoconstriction (HPV) response in preconstricted porcine PA. Porcine