A new study conducted at the University of Alabama at Birmingham suggested that potassium rich food like avocados and bananas might aid in protection against hardening of the arteries, also mentioned as pathogenic vascular calcification.
© Crevis / Shutterstock.com
This study is the first of this kind to use a mouse model to indicate that decreased dietary potassium leads to increased aortic stiffness.
In human beings, this kind of arterial stiffness has the potential to cause cardiovascular diseases and related deaths, and is considered as a vital health issue across the nation.
The study also found that an elevation in the levels of dietary potassium decreased aortic stiffness and vascular calcification.
The study enabled the researchers to investigate the underlining molecular mechanism of the impacts of high or low dietary potassium. This pointed out the need for considering consumption of dietary potassium for preventing vascular complications related with atherosclerosis. Also, the study reveals possibilities for novel treatment methods to treat or prevent arterial stiffness and atherosclerotic vascular calcification.
In order to analyze the underlying mechanism, the team used three methods— (a) living mice fed with diets of different potassium levels; (b) examining cross-sections of mouse artery in culture medium of different potassium concentrations; (c) vascular smooth muscle cells of mouse grown in culture medium.
The study used the atherosclerosis-prone mouse model that involves apoliprotein E-deficient mice; this is a standard animal model, which when fed with high-fat diet, is prone to heart disease.
The mice were provided either with low (0.3%), normal (0.7%) or high (2.1%) levels of dietary potassium based on a weight/weight scale.
The findings showed a noteworthy rise in vascular calcification in the mice fed with a low-potassium diet. However, a significant inhibition of the condition was evident in the mice fed with a high-potassium diet.
Pulse wave velocity — an arterial stiffness indicator that is calculated by echocardiography in live animals — was used by the researches to determine the aortic stiffness. The resultant data indicated an increased aortic stiffness in low-potassium mice and decreased stiffness in high-potassium mice.
In the three mice groups, the level of potassium in the blood represented the varied levels of dietary potassium.
The analyses of arterial cross-sections in potassium cultures suggested a direct impact on arterial calcification within arterial rings based on normal physiological blood potassium levels. While high-potassium suppressed aortic calcification in arterial rings, low-potassium increased calcification.
Paul Sanders, M.D., professor of nephrology in the UAB Department of Medicine and a co-author of the study commented that as the study findings validate the advantage of adequate potassium supplementation in preventing vascular calcification in atherosclerosis-prone mice, and points out the negative impacts of low potassium consumption, it has vital translational potential.
Additionally, the analyses made on cell culture also indicated an increase in calcification of the vascular smooth muscle cells.
Prior research had suggested similarities between calcification of vascular smooth muscle cells and the differentiation of bone cells that leads to the change of these smooth muscle cells into bone-like cells.
Consequently, the team evaluated the impact of mounting vascular smooth muscle cells in cell culture of low-potassium. It was found that in the low-potassium conditions, the expression of various gene markers related with bone cells were promoted.
However, under low-potassium conditions, the expression of vascular smooth muscle cell markers was decreased, which suggested the transformation of these cells into bone-like cells.
In order to identify that intracellular calcium in the vascular smooth muscle cells get elevated by low-potassium, the researchers used an inward rectifier potassium channel. Also, the activation of various known downstream mediators such as CREB (the calcium-activated cAMP response element-binding protein) and protein kinase C was carried out.
In low-potassium cells, autophagy (the intracellular degradation system) was increased by the activation of CREB. The researchers demonstrated that autophagy inhibitors can block calcification by blocking autophagy.
The researchers further tested the roles of autophagy signals as well as CREB activation in living-mouse models and the mouse artery cross-section in varied potassium concentrations. The results from both the tests confirmed the role for potassium in regulating vascular calcification via calcium signaling, autophagy and CREB.