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.
Download PDF:
Keywords: saturated and unsaturated free fatty acids, cholesterol, essential hypertension
Citation:
Titov V.N. (1998) Blockade of saturated fatty acids transport to a cell : pathogenesis of essential hypertension. Voprosy Meditsinskoi Khimii, 44(4), 317-330.
et al. Blockade of saturated fatty acids transport to a cell : pathogenesis of essential hypertension // Voprosy Meditsinskoi Khimii. - 1998. - V. 44. -N 4. - P. 317-330.
et al., "Blockade of saturated fatty acids transport to a cell : pathogenesis of essential hypertension." Voprosy Meditsinskoi Khimii 44.4 (1998): 317-330.
Titov, V. N. (1998). Blockade of saturated fatty acids transport to a cell : pathogenesis of essential hypertension. Voprosy Meditsinskoi Khimii, 44(4), 317-330.
Huff M. W., Miller D.B., Wolfe B.M., Connekky Ph. W. (1997) J.Lipid Res. 38. 1318 - 1333. Scholar google search
Ощепкова Е.В.(1995) Мягкая артериальная гипертония и патология магистральных артерий головы. Автореф. диссер. докт. мед. наук. М. Scholar google search
Chung В.Н, Tallis G.A., Cho В. Y.S., Segrest J.P. Henkin Y. (1995) J.Lipid Res. 36. 1956 - 1970. Scholar google search
Anel A., Richieri G. V., Kleinfelder A.M. (1993) Biochemistry. 32. 530 - 536. Scholar google search
Kuo P., Weinfeld M., Loscalzo J. (1990) Biochemistry. 29. 6626 - 6632. Scholar google search
Титов В.Н. (1980) Механизмы развития гиперлипопротеинемии при действии глюкокортикоидов и эстрогенов .Автореф. диссерт. докт. мед. наук, М. Scholar google search
Tamura M., Inagami Т., Kinoshita Т., Kuvano H. (1987) Hypertension. 5. 219 - 225. Scholar google search
Ng L.L., Sweeney E.P., Sizzovski M. (1995) Hypertension .25. 971 - 977. Scholar google search
Siffert W., Rosskopf D., Moritz A. (1995) J. Clin. Invest. 96. 759 - 766. Scholar google search
Titov V.N. (1997) Absrt. XI1 Eur. Congress Clin. Chem. Basel. August 17 - 22. Switzerland. 254. D 35. Scholar google search
Титов В.Н, Осипов СТ., Румянцев AT (1988) Лаб. дело. 9. 41 - 46. Arteriosclerosis. 7. 197 - 202. Scholar google search
