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NKCC2 is a transmembranous protein that facilitates the cotransport of 1 Na+, 1 K+, and 2 Cl- from extracellular fluid into the cell. The most common site for this membrane transporter lies on the apical surface of the thick ascending limb of the loop of Henle in the kidney. It is also found some places in the Brain.

In the Kidney this transporters acts to reabsorb Na+ and dilute the urine, decreasing the urines osmalarity to facilitate reabsorption of water in the distal tubule and collecting duct under the influence of Antidiuretic Hormone or Arginine Vasopressin Hormone.

NKCC2 is blocked by Furosemide which causes a more dilute urine by increasing the amount of Na+ excreted in the urine.

Many biological processes depend on maintaining differing concentrations of ions between the interior and exterior of cells. One way this is accomplished is through the action of "pump" or "transporter" molecules, that actively move ions in one direction or another across the cell membrane. Perhaps the best known of these is the "sodium pump", Sodium-potassium ATPase.

The Na-K-2Cl cotransporter is a carrier protein that transports Na+, K+, and Cl- into the cell in a stoichiometry of 1Na(+):1K(+):2Cl(-). There are two known isoforms, NKCC1 and NKCC2, each of which is present in different tissues and has distinct actions.

NKCC1 is expressed in many regions of the brain during early development but not in adulthood. This change in NKCC1 presence may be responsible for altering responses to the neurotransmitters GABA(A) and glycine from excitatory to inhibitory, which is likely to be crucial for early neuronal development and is an active area of neuroscience research. NKCC1 mediates this switch by raising internal Cl- concentrations in neurons, which is important to GABA and glycine responses as the respective ligand-gated anion channels are permeable to Cl-. When Cl- concentrations are much higher internally than externally (with respect to the cell) there is a large driving force outward on Cl-. Opening a channel to Cl- under these conditions will result in negative charge leaving the neuron, thereby depolarizing it, which is by definition excitatory. Put another way, increasing internal Cl- concentration increases the reversal potential for Cl- (by the Nernst Equation).

It has been suggested that the levels of NKCC1 and NKCC2 in some Neuroendocrine cells are dynamically regulated, leading to modulation of the chloride reversal potential, and thus the responsiveness of these cells to GABA.

NKCC2 is expressed in the kidney (in the ascending loop of Henle) and is crucial to proper fluid/ion retention and is inhibited by loop diuretics. An NKCC2 is also known as a BSC1 (bumetanide-sensitive cotransporter)

See also

• symporter

External links

• MeSH Sodium-Potassium-Chloride+Symporters

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