Potassium-Switch Signaling Pathway Dictates Acute Blood Pressure Response to Dietary Potassium

Mar 11, 2024Hypertension (Dallas, Tex. : 1979)

How a Potassium-Controlled Signal Pathway Affects Short-Term Blood Pressure Response to Dietary Potassium

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Abstract

Lower potassium levels in control mice resulted in progressively increased blood pressure and sodium retention.

As potassium levels decreased in control mice, blood pressure increased and became sensitive to dietary sodium and hydrochlorothiazide.
Increased phosphorylation and activity of the sodium-chloride cotransporter (NCC) were observed in response to low potassium.
Genetically altering mice to lock the potassium switch on resulted in consistently elevated blood pressure and sodium retention, unaffected by potassium changes.
The findings suggest that a low potassium diet, common in processed foods, activates the potassium switch pathway, leading to increased sodium retention and blood pressure.

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BACKGROUND: Potassium (K)-deficient diets, typical of modern processed foods, increase blood pressure (BP) and NaCl sensitivity. A K-dependent signaling pathway in the kidney distal convoluted tubule, coined the Kswitch, that couples extracellular Ksensing to activation of the thiazide-sensitive NaCl cotransporter (NCC) and NaCl retention has been implicated, but causality has not been established. + + + +

METHODS: To test the hypothesis that small, physiological changes in plasma K(P) are translated to BP through the switch pathway, a genetic approach was used to activate the downstream switch kinase, SPAK (SPS1-related proline/alanine-rich kinase), within the distal convoluted tubule. The CA-SPAK (constitutively active SPS1-related proline/alanine-rich kinase mice) were compared with control mice over a 4-day Ptitration (3.8-5.1 mmol) induced by changes in dietary K. Arterial BP was monitored using radiotelemetry, and renal function measurements, NCC abundance, phosphorylation, and activity were made. + + K+ K+

RESULTS: As Pdecreased in control mice, BP progressively increased and became sensitive to dietary NaCl and hydrochlorothiazide, coincident with increased NCC phosphorylation and urinary sodium retention. By contrast, BP in CA-SPAK mice was elevated, resistant to the Ptitration, and sensitive to hydrochlorothiazide and salt at all Plevels, concomitant with sustained and elevated urinary sodium retention and NCC phosphorylation and activity. Thus, genetically locking the switch on drives NaCl sensitivity and prevents the response of BP to potassium. K+ K+ K+

CONCLUSIONS: Low K, common in modern ultraprocessed diets, presses the K-switch pathway to turn on NCC activity, increasing sodium retention, BP, and salt sensitivity. + +

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Potassium-Switch Signaling Pathway Dictates Acute Blood Pressure Response to Dietary Potassium

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