Implication of Na+ kinetics in PGI2 generation of cultured human vascular endothelial cells.

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The regulatory mechanism of prostacyclin (PGI2) generation and its enhancement by ouabain and monensin in cultured human vascular endothelial cells was investigated with references to the kinetics of Ca++ and Na+. Na+-K+ ATPase activity was assayed as ouabain-sensitive 86Rb uptake. Cytosolic free calcium ion concentration ([Ca++]i) was measured using fura-2. The kinetics of 45Ca of 22Na, and [Ca++]i preceded PGI2 generation. Ouabain inhibited Na+-K+ ATPase activity (inhibition of 22Na release and 86Rb uptake) and increased 22Na uptake, while monensin enhanced 22Na uptake and Na+-K+ ATPase activity at 2.5min after starting incubation. Both of these reagents decreased 45Ca release and increased 45Ca uptake (inhibition of Na+-Ca++ exchange systems) at 2.5min. And all of these effects were attenuated at 10min. Ouabain and monensin increased [Ca++]i. Through these results it was concluded that the enhanced PGI2 generation by ouabain or monensin was speculated to be brought about by the increased [Ca++]i and Ca++ uptake which was based on the decreased Ca++ release via the inhibition of Na+-Ca++ exchange systems, and that enhanced PGI2 generation might be autoregulated by the attenuation of increased [Na+]i, which was derived from the attenuation of ouabain-induced inhibition of Na+-K+ ATPase activity, or from the enhancement of monensin-induced increase of its activity.
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