Low-sodium diet induces atherogenesis regardless of lowering blood pressure in hypertensive hyperlipidemic miceReport as inadecuate




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This study investigated the influence of sodium restriction and antihypertensive drugs on atherogenesis utilizing hypertensive H low-density lipoprotein-receptor knockout mice treated or not with losartan Los or hydralazine Hyd and fed low-sodium LS or normal-sodium NS chow. Despite reducing the blood pressure BP of H-LS mice, the LS diet caused arterial lipid infiltration due to increased plasma total cholesterol TC and triglycerides TG. Los and Hyd reduced the BP of H-LS mice, and Los effectively prevented arterial injury, likely by reducing plasma TG and nonesterified fatty acids. Aortic lipid infiltration was lower in Los-treated H-LS mice H-LS+Los than in normotensive N-LS and H-LS mice. Aortic angiotensin II type 1 AT1 receptor content was greater in H-NS than H-LS mice and in H-LS+Hyd than H-LS+Los mice. Carboxymethyl-lysine CML and receptor for advanced glycation end products RAGE immunostaining was greater in H-LS than H-NS mice. CML and RAGE levels were lower in LS animals treated with antihypertensive drugs, and Hyd enhanced the AT1 receptor level. Hyd also increased the gene expression of F4-80 but not tumor necrosis factor-α, interleukin IL-1β, IL-6, IL-10, intercellular adhesion molecule-1 or cluster of differentiation 66. The novelty of the current study is that in a murine model of simultaneous hypertension and hyperlipidemia, the pleiotropic effect of chronic, severe sodium restriction elicited aortic damage even with reduced BP. These negative effects on the arterial wall were reduced by AT1 receptor antagonism, demonstrating the influence of angiotensin II in atherogenesis induced by a severely LS diet.



Author: Fernanda B. Fusco, Diego J. Gomes, Kely C. S. Bispo, Veronica P. Toledo, Denise F. Barbeiro, Vera L. Capelozzi, Luzia N. S. Furuk

Source: http://plos.srce.hr/



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