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Researchers at University of Alabama at Birmingham (UAB) in the US have shown, for the first time, that reduced dietary potassium promotes elevated aortic stiffness in a mouse model, as compared with normal-potassium-fed mice.
Such arterial stiffness in humans is predictive of heart disease and death from heart disease, they said.
Researchers, including Anupam Agarwal from UAB, also found that increased dietary potassium levels lessened vascular calcification and aortic stiffness. They unravelled the molecular mechanism underlying the effects of low or high dietary potassium. Such knowledge of how vascular smooth muscle cells in the arteries regulate vascular calcification emphasises the need to consider dietary intake of potassium in the prevention of vascular complications of atherosclerosis.
It also provides new targets for potential therapies to prevent or treat atherosclerotic vascular calcification and arterial stiffness.
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The researchers determined a causative link between reduced dietary potassium and vascular calcification in atherosclerosis, as well as uncovered the underlying pathogenic mechanisms. The animal work was carried out in the atherosclerosis- prone mouse model, the apoliprotein E-deficient mice, a standard model that are prone to cardiovascular disease when fed a high-fat diet.
Using low, normal or high levels of dietary potassium, the team found that the mice fed a low-potassium diet had a significant increase in vascular calcification. In contrast, the mice fed a high-potassium diet had markedly inhibited vascular calcification.
The low-potassium mice had increased stiffness of their aortas, and high-potassium mice had decreased stiffness, as indicated by the arterial stiffness indicator called pulse wave velocity, which is measured by echocardiography in live animals. The different levels of dietary potassium were mirrored by different blood levels of potassium in the three groups of mice.