Researchers have found that mice with low dietary potassium are more likely to experience vascular calcification, which is characteristic of atherosclerosis. This is major risk factor for heart disease.
Increasing dietary potassium, however, was found to reduce vascular calcification in the rodents, suggesting that a diet rich in potassium could help to prevent heart disease.
The research team - led by Yabing Chen, Ph.D., a professor of pathology at the University of Alabama at Birmingham (UAB) - recently reported their findings in JCI Insight.
Heart disease is the leading cause of death for both men and women in the United States, killing around 610,000 people in the country every year.
Atherosclerosis is a key risk factor for heart disease. In atherosclerosis, deposits of fat, cholesterol, calcium, and other substances accumulate in the arteries, forming what is referred to as "plaque." Plaque hardens over time, restricting blood flow to the heart.
The new research from Prof. Chen and colleagues suggests that potassium supplementation could be one way to help combat atherosclerosis and reduce the risk of heart disease.
Potassium and vascular calcification
Potassium is a mineral that is considered essential for the human body. It not only aids muscle contraction and nerve and cell function, but it also helps to regulate the heartbeat.
Spinach and other leafy greens, as well as potatoes, carrots, oranges, and grapefruit, are just some of the fruits and vegetables that are good sources of potassium. The mineral is also available as a dietary supplement.
For their study, the team fed mice high-fat diets supplemented with either low, normal, or high levels of potassium. The mice used were deficient in a protein called apolipoprotein E, which makes rodents more susceptible to atherosclerosis in response to a high-fat diet.
The researchers found that mice fed a low-potassium diet showed an increase in vascular calcification and greater arterial stiffness, while mice fed a high-potassium diet showed a significant reduction in both conditions.
The team also assessed the effects of varying potassium levels on cultured vascular smooth muscle cells from mice, as well as on cultured cross sections of mouse arteries.
Study has 'important translational potential'
The cell culture analysis revealed that through a potassium transport channel called the inward rectifier potassium channel, low-potassium conditions led to a rise in intracellular calcium in vascular smooth muscle cells.
Also, the team found that low potassium triggers the calcium-activated cAMP response element-binding protein (CREB), which increases autophagy - an intracellular degradation process - in cells.
By inhibiting autophagy, the researchers found that they were able to prevent calcification in vascular smooth muscle cells, indicating that autophagy plays a significant role in the calcification process.
Through their analysis of cultured cross sections of mouse arteries and dietary experiments in live mice, the researchers confirmed that low potassium may lead to vascular calcification via calcium signaling, CREB, and autophagy. Increasing potassium levels, however, could reduce these effects.
While human studies are now needed to demonstrate the efficacy of potassium against vascular calcification in humans, the researchers believe that their current findings show promise.
"The findings have important translational potential, since they demonstrate the benefit of adequate potassium supplementation on prevention of vascular calcification in atherosclerosis-prone mice, and the adverse effect of low potassium intake."
Study co-author Dr. Paul Sanders, UAB Department of Medicine