[Lipoprotein-dependent synthesis of prostacyclin in smooth muscle cells].
Low (LDL) and high density lipoproteins (HDL) stimulated prostacycline (PGI2) synthesis in rabbit and human aorta smooth muscle cells growing in culture. The lipoproteins were added to the cells in concentrations equal to that of cholesterol. It was shown that HDL exerted a stronger stimulating effect as compared to LDL. The maximal effect was observed with HDL3. HDL3 isolated from blood serum of healthy volunteers appeared to be more active in PGI2 synthesis promotion than those of CDH patients with documented coronary atherosclerosis. Purified Apo A-1 stimulated the transformation of [14C]arachidonic acid into the products of its metabolism with increased accumulation of 6-keto-PGF1 alpha among labeled metabolites. Estradiol (1.10(-7) M) showed a stimulating effect; norepinephrine (1.10(-6) M) and progesterone (1.10(-7) M) showed an inhibiting effect, whereas corticosterone (1.10(-6) M) and deoxycorticosterone (1.10(-6) M) did not influence the rate of LDL-dependent PGI2 synthesis.
D000818:Animals; D001011:Aorta / Q000378:metabolism; D016632:Apolipoprotein A-I; D001054:Apolipoproteins A / Q000502:physiology; D016718:Arachidonic Acid; D001095:Arachidonic Acids / Q000378:metabolism; D002478:Cells, Cultured; D003327:Coronary Disease / Q000097:blood / Q000378:metabolism; D011464:Epoprostenol / Q000096:biosynthesis*; D006801:Humans; D008075:Lipoproteins, HDL / Q000097:blood / Q000502:physiology*; D008077:Lipoproteins, LDL / Q000097:blood / Q000502:physiology*; D008297:Male; D009131:Muscle, Smooth, Vascular / Q000378:metabolism*; D011817:Rabbits
D016632:Apolipoprotein A-I; D001054:Apolipoproteins A; D001095:Arachidonic Acids; D008075:Lipoproteins, HDL; D008077:Lipoproteins, LDL; D016718:Arachidonic Acid; D011464:Epoprostenol
Lipoproteidzavisimyĭ sintez prostatsiklina v gladkomyshechnykh kletkakh.