Hypoxia activates a background conductance in freshly isolated pulmonary arterial endothelial cells of the rat

• Published in: FEBS letters 2002-07, Vol.522 (1), p.125-129
• Main Authors: Hogg, Dayle S, Kozlowski, Roland Z
• Format: Article
• Language: English
• Subjects: Amiloride - analogs & derivatives; Amiloride - pharmacology; Animals; Cell Hypoxia; Cells, Cultured; DCB, 2′,4′-dichlorobenzamil; E m, membrane potential; Electrophysiology; Endothelial cell; Endothelium, Vascular - cytology; Gadolinium - pharmacology; HEPES, N-2-hydroxyethylpiperazine-N-2-ethanesulfonic acid; HPV, hypoxic pulmonary vasoconstriction; Hypoxia; I NSC, non-selective cation current; I −90, mean current at −90 mV; I–V, current–voltage; Lanthanum - pharmacology; Male; Non-selective cation channel; Oxygen - metabolism; PAEC, pulmonary artery endothelial cells; Potassium Channels - drug effects; Potassium Channels - physiology; Pulmonary artery; Pulmonary Artery - cytology; Rats; Rats, Wistar; Sodium-Calcium Exchanger - antagonists & inhibitors
• ISSN: 0014-5793; 1873-3468
• DOI: 10.1016/S0014-5793(02)02912-5

Utilising the patch-clamp recording technique we have demonstrated for the first time the effects of hypoxia on the background current in pulmonary arterial endothelial cells. Electrophysiological studies revealed the presence of a novel oxygen-sensitive, non-selective cation conductance ( I NSC) in these cells. The inward component of I NSC was significantly potentiated by hypoxia. Both the inward and outward components of I NSC were inhibited by both La 3+ and Gd 3+. Hypoxic activation of I NSC may provide an important Ca 2+ influx pathway essential for the release of a pulmonary-selective vasoconstrictor pivotal to the sustained phase of hypoxic pulmonary vasoconstriction.