Research on the pathogenis and protection of Atherosclerosis

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1. Research on the Pathogenesis of Atherosclerosis: Proliferation of vascular smooth muscle cells (VSMC) and deposition of lipid is important for the pathogenesis of atherosclerosis.1) Vascular smooth muscle cells from rat aorta contaied a specific receptor for the 1,25-dihydroxyvitamin D_3 and it stimulated the proliferation and suppressed the synthesis of glycosaminoglycan.2) Platelet derived growth factor (PDGF) increased intracellular Ca^<2+> concentration ([Ca^<2+>] i) in rabbit chondrocytes and stimulated the synthesis of DNA and glycosaminoglycan. Suramin, an antagonist of PDGF, suppressed the increase of [Ca^<2+>] i and the synthesis of DNA.3) Low density lipoprotein (LDL) increased [Ca^<2+>] i. LDL caused a release of Ca^<2+> from intracellular Ca^<2+> store through production of inositole trisphosphate (iP_3).4) A specific receptor for PDGF existed in the basolateral membrane of dog kidney and PDGF stimulated Ca^<2+>- ATPase.2. Reaserch for the effects of various chemical compounds on the intracellular Ca^<2+> signal system.1) Prostaglandin F2 and angiotensin II (AII), both of which are strong vasoconstrictor, increased [Ca^<2+>] i in VSMC and caused the release of Ca^<2+> from intracellular Ca^<2+> store. Nicorandil, a vasodilator, suppressed the increase of [Ca^<2+>] i induced by prostaglandin F2 and AII.2) Valinomycin, a potassium ionophore, suppressed the release of CA^<2+> from intracellular Ca^<2+> store induced by AII but did not suppress those induced by ionomycin, a Ca^<2+> ionophore. However valinomycin did not sauppress the production of iP_3 induced by AII.3) Nitroglycerin and nicorandil, which are nitrates, stimulated the activities of Ca^<2+>-ATPase in the microsmal fraction of porcine coronary artery smooth muscle cells, but Ca^<2+> channel blockers did not.