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Dietary potassium regulates vascular calcification and arterial stiffness.


Maximus Peto’s Commentary

I have been pondering for years how the adequate daily intake for potassium seems so high ( up to 3.4 g/day for adult males ). The results of this study are remarkable: increased dietary potassium reduced vascular calcification and aortic stiffness, while low dietary calcium increased intracellular calcium. I wonder if the body uses calcium in place of potassium, when potassium is scarce. That vascular stiffness was altered is interesting; what implication might this have for the theory that AGE accumulation causes age-related vascular stiffness? Note that this study was done in a mutant mouse model of atherosclerosis (ApoE -/-).


Dietary potassium regulates vascular calcification and arterial stiffness.
JCI Insight. 2017 Oct 5;2(19). pii: 94920.
Sun Y, Byon CH, Yang Y, Bradley WE, Dell’Italia LJ, Sanders PW, Agarwal A, Wu H, Chen Y
DOI: 10.1172/jci.insight.94920
PubMed publication date (edat): 10/6/2017

Abstract

Vascular calcification is a risk factor that predicts adverse cardiovascular complications of several diseases including atherosclerosis. Reduced dietary potassium intake has been linked to cardiovascular diseases such as hypertension and incidental stroke, although the underlying molecular mechanisms remain largely unknown. Using the ApoE-deficient mouse model, we demonstrated for the first time to our knowledge that reduced dietary potassium (0.3%) promoted atherosclerotic vascular calcification and increased aortic stiffness, compared with normal (0.7%) potassium-fed mice. In contrast, increased dietary potassium (2.1%) attenuated vascular calcification and aortic stiffness. Mechanistically, reduction in the potassium concentration to the lower limit of the physiological range increased intracellular calcium, which activated a cAMP response element-binding protein (CREB) signal that subsequently enhanced autophagy and promoted vascular smooth muscle cell (VSMC) calcification. Inhibition of calcium signals and knockdown of either CREB or ATG7, an autophagy regulator, attenuated VSMC calcification induced by low potassium. Consistently, elevated autophagy and CREB signaling were demonstrated in the calcified arteries from low potassium diet-fed mice as well as aortic arteries exposed to low potassium ex vivo. These studies established a potentially novel causative role of dietary potassium intake in regulating atherosclerotic vascular calcification and stiffness, and uncovered mechanisms that offer opportunities to develop therapeutic strategies to control vascular disease.

PMID: 28978809
Free Full-Text: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5841863/

Maximus Peto

Max Peto is a longevity researcher and founder of Long Life Labs. A biochemist by training, he studies the biochemistry of aging and longevity and has worked with research organizations such as SENS Research Foundation, Methuselah Foundation, BioAge Labs, Life Extension Foundation, and Ichor Therapeutics. His work at Long Life Labs is focused on empowering people to understand and manage the most critical factors for better health and longer life.

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