AI Article Synopsis

  • Rats on a cholesterol-rich diet developed high levels of cholesterol and lipids in their serum, liver, and carcass, even though their bodies stopped making cholesterol.
  • Hypertension induced by desoxycorticosterone and salt further worsened cholesterol levels and led to atherosclerotic changes, while hypertension from renal artery constriction had a similar amplifying effect.
  • The severity of atherosclerotic lesions was linked to serum cholesterol levels, and there was a positive relationship between blood pressure and hypercholesterolemia, but it was unclear if the atherosclerosis was due to high lipid content or the impact of high blood pressure itself.

Article Abstract

Rats on a stock diet with added cholesterol, cholic acid, and thiouracil developed increased concentrations of cholesterol, total lipide, and beta lipoprotein in the serum, and an increased content of cholesterol in the liver and carcass, despite the fact that the diet produced a cessation of endogenous cholesterol synthesis. Rats with high serum lipide concentrations developed intimal lesions similar to those of human atherosclerosis. The induction of hypertension by desoxycorticosterone and salt accelerated the development of hypercholesterolemia, hyperlipemia, increase in tissue cholesterol content, and atherosclerotic changes in the intima. Hypertension induced by renal artery constriction also intensified the hypercholesterolemia and hyperlipemia. On the other hand, rats receiving desoxycorticosterone acetate without salt or salt without desoxycorticosterone acetate did not show any intensification of hypercholesterolemia or hyperlipemia. The extent of the atherosclerotic lesions was correlated with the concentration of cholesterol in the serum. There was also a positive correlation between blood pressure and the degree of hypercholesterolemia. It remained uncertain whether the increase in atherosclerosis in the hypertensive animals was dependent on the increased lipide content of serum and tissues or on a local effect of the elevated blood pressure.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2136835PMC
http://dx.doi.org/10.1084/jem.107.4.581DOI Listing

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