Endogenous Regulation of Prostacyclin Synthesis in Arterial Smooth Muscle Cells

Abstract

The physiological and pathological roles of prostacyclin* (PGI2) and thromboxane A₂ have attracted much attention in atherosclerosis. Many investigations support the hypothesis that the loss of balance between these two prostaglandins is involved in vascular disease.² The capacity of the vascular wall to produce PGI2 was reported originally for the intimal surface,³ but medial smooth muscle cells also produce significant quantities both in vivo⁴,⁵ and under culture conditions.⁶ This capacity seems to be of importance especially after endothelial injury, such a situation probably involved in the atherosclerotic process. Using arterial smooth muscle cells in culture, we have previously demonstrated that, in comparison with healthy cultured cells, cells originating from atherosclerotic aortas have a decreased capacity to produce PGI2.⁸ Such a reduced prostacyclin formation has been reported in aged aortic smooth muscle cells⁹ associated with an increased PGE2 synthesis. Despite this, the regulative mechanisms of PGI₂ generation in arterial cells remains unclear.