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1 University of Aarhus, The Water and Salt Research Center, Aarhus, Denmark; Institute of Anatomy, University of Aarhus, Aarhus, Denmark
2 University of Aarhus, The Water and Salt Research Center, Aarhus, Denmark; Department of Physiology, Dongguk University, Kyungju, Korea, Republic of
3 Renal Division, Emory University School of Medicine, Atlanta, GA, USA
4 Department of Medicine, University of Florida, Gainesville, FL, USA
5 University of Aarhus, The Water and Salt Research Center, Aarhus, Denmark; Institute of Experimental Clinical Research, University of Aarhus, Aarhus, Denmark
* To whom correspondence should be addressed. E-mail: sn{at}ana.au.dk.
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 rats (n=6). Rats treated with lithium for 28 days showed decreased urine pH, whereas no significant differences in blood pH and plasma HCO3- levels were observed. Immunoblot anaylsis revealed that lithium treatment induced a significant increase in the expression of the H+-ATPase (B1-subunit) in cortex (190 ±18%), 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 AE1 (400 ± 40%). This was confirmed by immunocytochemistry and immunoelectron microscopy which also revealed increased density of intercalated cells. Moreover, immunoblotting and immunocytochemistry also revealed a significant increase in the expression of the electrogenic NBC1 in cortex (200 ± 23%) and of the electroneutral NBCn1 in inner stripe of outer medulla (250 ± 54%). In contrast, there were no changes in the expression of NHE3 or of the Cl-/HCO3- 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 bicarbonate reabsorption, ammonium reabsorption, and proton secretion to prevent the development of systemic metabolic acidosis.
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