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Macrophage SPAK deletion limits a low potassium-induced kidney inflammatory program.

Am J Physiol Renal Physiol

November 2024

Division of Nephrology, Department of Medicine, Vanderbilt University Medical Center, Nashville, Tennessee, United States.

Inadequate dietary potassium (K) consumption is a significant contributor to poor cardiovascular outcomes. A diet with reduced K content has been shown to cause salt-sensitive increases in blood pressure. More recently, we have also shown that reductions in blood K can cause direct kidney injury, independent of dietary sodium (Na) content.

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Phosphorylation of Ser19 (S19-p) on the myosin regulatory light chain (MLC2) is critical for arterial contraction. It has been shown that elevated RhoA-dependent kinase (ROCK) activity or decreased MLC phosphatase (MLCP) activity leads to further phosphorylation of Thr18 (T18/S19-pp), which has been linked to vasospastic diseases. However, this phenomenon has not yet been studied in the context of pulmonary arterial hypertension (PAH).

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High sodium and low potassium intake have both been linked to poor cardiovascular health outcomes and increased mortality rates. A combination of the two is thought to be particularly detrimental. While mechanisms are multiple, the kidney is an important target of harmful effects and low potassium influences on both proximal and distal nephron segments are especially potent.

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