In mice eating normal salt, even though extra potassium slows down one salt-handling channel (NCC), it doesn't lower blood pressure because another channel (ENaC) starts pulling in more salt instead.
Scientific Claim
On a normal salt diet, dietary potassium intake above 1.75% does not lower blood pressure despite reducing NCC activity, indicating that ENaC-mediated sodium reabsorption may counteract NCC-related benefits in male mice.
Original Statement
“However, we found that at the 4–5-day timepoint where BP was recorded, none of the dietary intakes had the capacity to reduce BP, and therefore, we did not extend the dietary feeding period further. Instead, dark phase SBP remained relatively stable up to a 1.5% K+ intake, then was significantly increased from the 1.75% K+ intake and above.”
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 descriptive claims about physiological outcomes. The language accurately reflects observed data without causal implications.
Evidence from Studies
Supporting (1)
Excess dietary potassium raises blood pressure in male mice by an aldosterone-dependent increase in ENaC