Abstract
See related article, pp 904–912 The thiazide-sensitive Na/Cl cotransporter NCC mediates NaCl reabsorption by the distal convoluted tubule (DCT) playing an important role in Na homeostasis and blood pressure regulation. In addition, the DCT is involved in maintaining K+ homeostasis by controlling the amount of K+ secreted into the lumen through the apical channel ROMK (renal outer medulla K+ channel).1 NH2-terminal NCC phosphorylation by SPAK (STE20-related proline–alanine rich kinase) kinases is known to stimulate NCC activity. It is well established that chronically elevated angiotensin II (Ang II) increases NCC phosphorylation, and this thought to be mediated in part by activation of SPAK kinases. Several lines of evidence indicate that WNK (with-no-lysine kinase) kinases are upstream of SPAK and involved in Ang II–induced stimulation of NCC phosphorylation. However, recent data point to an important role of plasma potassium in the regulation of NCC phosphorylation that may override NCC regulation by hormones and dietary salt. For example, acutely increasing plasma K+ in rats decreased …
Highlights
From the Hypertension and Vascular Research Division, Department of Internal medicine, Henry Ford Hospital, Detroit, MI
These data point to a kaliuretic effect of Ang II infusion with potential depletion of overall K+ stores, which is evident after fasting rats and restored by high-K+ diet
The authors describe that Ang II infusion induces kaliuresis in rats fed 1% K+ diet, and this is tripled in rats fed 2% K+ diet without any significant changes on plasma K+
Summary
It is unclear whether a meal containing high-K+ content is sufficient to affect NCC phosphorylation and to which extent an increase in plasma K+ is required to decrease NCC phosphorylation. Veiras et al[8] studied whether a single meal containing 2% K+ induced kaliuresis in control or Ang II–induced hypertensive rats. The high-K+ meal did not induced kaliuresis despite normalizing plasma K+.
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
