Abstract
In bovine pulmonary artery endothelial cells, ionic currents and the concentration of free intracellular Ca2+ ([Ca2+]i) were measured with a combined patch clamp and Ca2+-fluorimetric method (Fura-2). Volume-activated Cl––currents (ICl,vol) were activated by a 13 or 28% decrease in tonicity. Thrombin, 1 U/ml, strongly potentiated ICl,vol preactivated by low hypotonicity (13% HTS) but had no effect on ICl,vol preactivated by stronger hypotonic challenges (28% HTS). The thrombin-induced potentiation was not affected by buffering [Ca2+]i at 50–100 nmol/l and omitting extracellular Ca2+. A peptide agonist of the thrombin receptor, SFLLRN, also potentiated ICl,vol, while an enzymatically inactive thrombin analogue, DIP-thrombin, was without effect. These results suggest that proteolytic activation of the thrombin receptor sensitises the activation of ICl,vol in endothelial cells in a Ca2+-independent mechanism.
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Received: 27 September 1996 / Received after revision: 16 January 1997 / Accepted: 30 January 1997
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Manolopoulos, G., Prenen, J., Droogmans, G. et al. Thrombin potentiates volume-activated chloride currents in pulmonary artery endothelial cells. Pflügers Arch 433, 845–847 (1997). https://doi.org/10.1007/s004240050354
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DOI: https://doi.org/10.1007/s004240050354