Modulation of prostacyclin generation in cultured human vascular endothelial cells and the effects of human alpha-natriuretic polypeptide.

Vascular endothelial cells have been known to possess not only a barrier function but also other biologically important functions maintaining vascular homeostasis. Among these, the generation of prostacyclin is one of the most conspicuous functions, and the modulation of its synthesis and liberation has been of interest with reference to the interaction with several vasoactive substances, including human atrial alpha-natriuretic polypeptide. This paper investigates the regulatory mechanism of prostacyclin generation using cultured human vascular endothelial cells as far as Ca2+ flux, (Na+ + K+)-ATPase activity, and Na+-Ca2+ exchange systems are concerned. Through these experimental studies the following results were obtained. Prostacyclin generation was triggered by an increase of Ca2+ influx, and an increase in intracellular Na+ also enhanced it, and this was accompanied by a decreased Ca2+ efflux arising from suppression of Na+-Ca2+ exchange systems. (Na+ + K+)-ATPase activity as well as prostacyclin generation was also enhanced by the increase of intracellular Na+. These results indicate a possible link between the mechanism which generates prostacyclin in the human vascular endothelial cells and the mobilization of electrolytes; however, in this aspect human atrial alpha-natriuretic polypeptide had no effect on the endothelial cells.