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1 Water and Salt Research Center, University of Aarhus, Denmark; Department of Anatomy, University of Aarhus, Denmark
2 Water and Salt Research Center, University of Aarhus, Denmark; Department of Biochemistry and Cell Biology, School of Medicine, Kyungpook National University, Korea, Republic of
3 Water and Salt Research Center, University of Aarhus, Denmark; Institute of Clinical Medicine, Aarhus University Hospital, United States
4 Water and Salt Research Center, University of Aarhus, Institute of Anatomy, United States; Department of Anatomy, University of Aarhus, Denmark
* To whom correspondence should be addressed. E-mail: sn{at}ana.au.dk.
The purpose of the present studies was to determine the effects of high dose aldosterone and dDAVP treatment on renal AQP2 regulation and urinary concentration. Rats were treated for six days with either vehicle (CON, n=8), dDAVP 0.5ng/h (dDAVP, n=10), aldosterone (ALDO, 150ug/d, n=10) or combined dDAVP and aldosterone treatment (dDAVP+ALDO, n=10) and had free access to water with a fixed food intake. Aldosterone treatment induced hypokalemia, decreased the urine osmolality and increased the urine volume and water intake when comparing ALDO to CON and comparing dDAVP+ALDO to dDAVP. Immunohistochemistry and semiquantitative laser confocal microscopy revealed a distinct increase in basolateral domain AQP2 labeling in CCD principal cells and a reduction in apical domain labeling in ALDO compared to CON. Given the presence of hypokalemia in aldosterone treated rats, we studied dietary induced hypokalemia in rats which also reduced apical AQP2 expression in the CCD but did not induce any increase in basolateral AQP2 expression in the CCD as observed with aldosterone treatment. The aldosterone induced basolateral AQP2 expression in the CCD was thus independent of hypokalemia but was dependent on the presence of sodium and aldosterone. This redistribution was clearly blocked by mineralocorticoid receptor blockade. The increased basolateral expression of AQP2 induced by aldosterone may play a significant role for water metabolism in conditions with increased sodium reabsorption in the CCD.
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