Abstract
Recently the involvement of PGI2 or Ca++ has been discussed in reference to the development of atherosclerosis.
We, therefore, investigated the relationship between the intra- and extra-cellular Ca++ and PGI2 generation using cultured human vascular endthelial cells. Endothelial cells were isolated from human umbilical cord and cultured by the modified method of Jaffe et al. 6-keto PGF1α content in the supernatant over the monolayer cells was used as the parameter of PGI2 generation. The net influx of Ca++ was calculated by counting the radioactivity of the incorporated Ca45 (5μCi/ml) in the endothelial cells.
The obtained results are as follows: 1) Calcium ionophore A23187 (10-6, 10-5M) enhanced PGI2 generation in a dose dependent manner. 2) The enhanced PGI2 generation by A23187 was abolished in the Ca++ free medium. 3) Intracellular Ca++ immobilizer TMB-8 (10-3M) abolished PGI2 generation induced by A23187. 4) The net influx of Ca45 increased parallel with the PGI2 generation. 5) A23187 enhanced the net influx of Ca45, 1.7 fold.
These results suggest that the enhancement of PGI2 generation is originated from the increased cytosolic free Ca++ by an influx of extracellular Ca++ or a release of Ca++ from the storage site. And it is concluded that suspected Ca++ influx into vascular endothelial cells during development of atherosclerosis could enhance PGI2 generation as one of the protective factors for atherosclerosis.
