High K diets prevent hypertensive endothelial injury and intimal thickening.
Cholesterol esters often deposit during
hypercholesterolemia. Would a high K diet influence
cholesterol ester deposits? In a normal rat on a normal diet, no
cholesterol esters are detected in the aorta.
Stroke prone SHR rats were fed for 3 months a basic diet containing 4%
cholesterol, 14%
coconut oil and 7% NaCl. One group of 13 rats had normal (.5%) K in the diet. Another group of 10 rats ate high (2.1%) K. Mean intraarterial blood pressures averaged 165 mm Hg in the normal K group and 161 mm Hg in the high K group (P = NS). The serum
cholesterol averaged 229 mg/dL in the normal K group and 214 in the high K group (P = NS). Total aortic
cholesterol esters per rat involving 16 and 18
carbon chain
fatty acids averaged 187 micrograms in normal K v 68 micrograms in high K, measured by gas chromatography. These were the main
esters; other
esters were negligible. Thus high K reduced
cholesterol ester deposits by 64% (P less than .0003), even though blood pressure and
cholesterol levels were quite similar in the two groups. Both high
cholesterol and high BP injure endothelial cells and increase invasion of macrophages and vascular smooth muscle cells into the intima and increase endothelial permeability to
proteins. With high plasma
cholesterol, these processes lead to
atherosclerosis with
cholesterol ester deposition. The high K diet, by protecting endothelial cells, can greatly decrease this
cholesterol ester deposition. This effect could possible be useful for preventing atherosclerotic complications such as
heart attacks in human
hypertension.