August 7, 2014Journal of Hypertension

Posttranslational regulation of the cation–chloride symporter Na+–K+–2Cl− cotransporter-2 in spontaneously hypertensive rat kidneys

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Structured PICO

Population

Spontaneously hypertensive rats (SHR), normotensive Wistar-Kyoto rats (WKY), and human embryonic kidney (HEK) cells

Intervention

Overexpression of Na+-K+-ATPase β1 subunit (β1NK)

Comparator

Normotensive Wistar-Kyoto rats (WKY) and baseline HEK cells

Outcome

NKCC2 cell-surface expression and ion transport activitysurrogate

Limitations

Uncertain translation from transfected HEK cells to native renal tissue
Lack of physiological polarity in membrane expression of NKCC2 and β1NK in transfected HEK cells

Discussion

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Implication

This editorial highlights new preclinical evidence that the Na+-K+-ATPase β1 subunit interacts with NKCC2 to increase its surface expression, potentially contributing to renal sodium retention in hypertension.

Cite This Study

Olaf Grisk (2014) studied this question.

synapsesocial.com/papers/6a7dcaaa1ec832c82ccdb005 https://doi.org/10.1097/hjh.0000000000000303

Topics

Hypertension management

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Posttranslational regulation of the cation–chloride symporter Na+–K+–2Cl− cotransporter-2 in spontaneously hypertensive rat kidneys

Structured PICO

Limitations

Discussion

Implication

Cite This Study

Topics

Posttranslational regulation of the cation–chloride symporter Na+–K+–2Cl− cotransporter-2 in spontaneously hypertensive rat kidneys

Structured PICO

Limitations

Discussion

Implication

Cite This Study

Also Consider

Topics

Also Consider