What can we learn from erythrocyte Na–K–Cl cotransporter NKCC1 in human hypertension?  Ricardo P. Garay, Octavio Alda  Pathophysiology  Volume 14, Issue 3, Pages 167-170 (December 2007) DOI: 10.1016/j.pathophys.2007.09.006 Copyright © 2007 Elsevier Ireland Ltd Terms and Conditions

Fig. 1 NKCC1 function in erythrocytes and vascular smooth muscle cells. NKCC1 moves 1Na+, 1K+ and 2Cl− ions into the cell interior (inward cotransport) and also out of the cell (outward cotransport). In human erythrocytes under physiological conditions, inward and outward cotransport are of similar magnitude, i.e.: hNKCC1 is silent (in equilibrium). Conversely, in vascular smooth muscle cells inward cotransport is faster than outward cotransport, providing a net entry of Na+, K+ and Cl− ions into the cell interior (net means difference between the unidirectionals outward and inward cotransport). The explanation of these differences is simple. Cotransport fluxes are entirely passive (without ATP hydrolysis) and only governed by the electrochemical gradients, i.e.: by the inward sodium gradient accross the vascular smooth muscle cell membrane (which functions as a “potassium electrode”) and by the (similar) inward sodium and outward potassium gradients across the mammal erythrocyte cell membrane (which functions as a “chloride electrode”). Pathophysiology 2007 14, 167-170DOI: (10.1016/j.pathophys.2007.09.006) Copyright © 2007 Elsevier Ireland Ltd Terms and Conditions