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Hyperosmotic but not Hyposmotic Stress Evokes a Rise in Cytosolic Ca 2+ Concentration in Endothelium of Intact Rat Aorta
Author(s) -
Marchenko Sergey M.,
Sage Stewart O.
Publication year - 2000
Publication title -
experimental physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.925
H-Index - 101
eISSN - 1469-445X
pISSN - 0958-0670
DOI - 10.1111/j.1469-445x.2000.01943.x
Subject(s) - osmotic concentration , extracellular , mechanosensitive channels , endothelium , cytosol , medicine , osmotic shock , intracellular , endocrinology , chemistry , biophysics , aorta , biology , biochemistry , ion channel , receptor , gene , enzyme
The effects of osmotic stress on the cytosolic Ca 2+ concentration ([Ca 2+ ] i ) in the endothelium of excised intact rat aorta were investigated using the indicator fura‐2 and the patch clamp technique. Hyperosmotic stress evoked a reversible rise in endothelial [Ca 2+ ] i in the presence but not absence of extracellular Ca 2+ , indicating that it evoked Ca 2+ entry without release from intracellular stores. Hyposmotic stress was without significant effect. Cytochalasins B and D reduced the effect of hyperosmotic stress but not acetylcholine on endothelial [Ca 2+ ] i . In endothelium isolated from underlying smooth muscle, hyperosmotic stress produced a rise in the [Ca 2+ ] i and depolarisation of the endothelial membrane potential whereas hyposmotic stress was without effect. Mechanosensitive cationic channels recorded in cell‐attached patches were activated by hyperosmotic solutions applied to the endothelium and inhibited by hyposmotic solutions. These data suggest that shrinkage of endothelial cells evokes an increase in [Ca 2+ ] i by opening a pathway for Ca 2+ entry from the extracellular space. The mechanosensitive ionic channels which we have previously described may be responsible for this response.