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1The Water and Salt Research Center, Institutes of 2Anatomy and 6Experimental Clinical Research, University of Aarhus, DK-8000 Arahus C, Denmark; 3Department of Physiology, School of Medicine, Dongguk University, Kyungju 780-714, Korea; 4Renal Division, Emory University School of Medicine, Georgia 30322; 5Department of Medicine, University of Florida, Gainesville, Florida 32610-0215
Submitted 6 May 2003 ; accepted in final form 14 August 2003
Prolonged lithium treatment of humans and rodents often results in hyperchloremic metabolic acidosis. This is thought to be caused by diminished net H+ secretion and/or excessive back-diffusion of acid equivalents. To explore whether lithium treatment is associated with changes in the expression of key renal acid-base transporters, semiquantitative immunoblotting and immunocytochemistry were performed using kidneys from lithium-treated (n = 6) and control (n = 6) rats. Rats treated with lithium for 28 days showed decreased urine pH, whereas no significant differences in blood pH and plasma 
levels were observed. Immunoblot analysis revealed that lithium treatment induced a significant increase in the expression of the H+-ATPase (B1-subunit) in cortex (190 ± 18%) and inner stripe of the outer medulla (190 ± 9%), and a dramatic increase in inner medulla (900 ± 104%) in parallel to an increase in the expression of type 1 anion exchanger (400 ± 40%). This was confirmed by immunocytochemistry and immunoelectron microscopy, which also revealed increased density of intercalated cells. Moreover, immunoblotting and immunocytochemistry revealed a significant increase in the expression of the type 1 electrogenic 
cotransporter (NBC) in cortex (200 ± 23%) and of the electroneutral NBCn1 in inner stripe of the outer medulla (250 ± 54%). In contrast, there were no changes in the expression of Na+/H+ exchanger-3 or of the 
exchanger pendrin. These results demonstrate that the expression of specific renal acid-base transporters is markedly altered in response to long-term lithium treatment. This is likely to represent direct or compensatory effects to increase the capacity for reabsorption, 
reabsorption, and proton secretion to prevent the development of systemic metabolic acidosis.
acid-base balance; distal tubular acidosis; hydrogen ion-adenosinetriphosphatase; electroneutral 
co-transporter; pendrin
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