When mice don't get enough potassium, their kidney transporter becomes more active and blood pressure rises, but a common blood pressure drug can lower it again.

Scientific Claim

Dietary potassium depletion in mice is associated with increased sodium-chloride cotransporter (NCC) activity and elevated blood pressure, and thiazide diuretic administration is associated with reduced blood pressure in potassium-depleted mice.

Original Statement

“BP was significantly higher in mice receiving a 0K diet for 2 weeks relative to mice receiving a NK diet. BP was further increased during concurrent high NaCl intake. This increase in BP was associated with increased total and pNCC but with reduced ENaC abundance. HCTZ reduced the BP of HS/0K-fed mice back to the levels observed in HS/NK-fed animals.”

From study:Dissociation of sodium-chloride cotransporter expression and blood pressure during chronic high dietary potassium supplementation

Evidence Quality Assessment

Claim Status

appropriately stated

Study Design Support

Design supports claim

Appropriate Language Strength

association

Can only show association/correlation

Assessment Explanation

The study design supports correlational claims. The phrasing uses 'associated with' for both NCC activity and thiazide effects, correctly avoiding causal language.

Evidence from Studies

Supporting (1)

Dissociation of sodium-chloride cotransporter expression and blood pressure during chronic high dietary potassium supplementation

Cohort Study

Animal

2023 Mar 8

Contradicting (0)

No contradicting evidence found

Source Study

Dissociation of sodium-chloride cotransporter expression and blood pressure during chronic high dietary potassium supplementation

Score: 13

DOI: 10.1172/jci.insight.156437

Similar Assertions

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