Voprosy meditsinskoi khimii (ISSN 0042-8809)

Blockade of saturated fatty acids transport to a cell : pathogenesis of essential hypertension

   
Titov V.N.
PubMed Id: 9845918
Year: 1998 vol: 44  issue:4  pages: 317-330
Abstract: Increased resistance to blood flow in arteries is built up by blockadeof transport of saturated fatty acids of triglycerides in VLDL to cell through apoE/B-100receptor endocythosis (active transport). This way does not affect the structure of cellmembrane. blockade of the active transport stimulates the compensating activation oflipolysis increasing the level of free saturated fatty acids in the blood. These fattyacids are included into the cell membrane via passive transport. In the membrane fattyacids form local domains with unregulated permeability and nonspecific ion transport: Na+and Ca2+ enter into cell without any control and K+ and Mg2+leak out. Responding cells activate Na+, K+- and Ca2+-ATPase and cholesterol synthesis. Ion pumps activate Na+ and Ca2+out-fluxes; cholesterol blocks nonspecific ion permeability, but increases membranemicroviscosity and inhibits secondary activity of ion pumps, thus forming vicious circleof hypernatriemia and hypercalciemia disturbing functions of loose conective tissue. Theyincrease cell size, promote synthesis and secretion of collagen and elastin.lt has led towail thickening, elasticity drop and artety clear cross section narrowing. The increase ofsensitivity to contractility of smooth muscle cells, hyperreactivity towards pressorregulators and resistance to depressor regulators cause artery spasm, peripheralresistance increases and starts up pathogenesis of essential hypertension.
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Reference: Titov V.N., Blockade of saturated fatty acids transport to a cell : pathogenesis of essential hypertension, Voprosy meditsinskoi khimii, 1998, vol: 44(4), 317-330.
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