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1 Department of Biochemistry and Cell Biology, School of Medicine, Kyungpook National University, Taegu, Korea, Republic of
2 Taegu, Korea, Republic of; Department of Biochemistry and Cell Biology, School of Medicine, Kyungpook National University, Taegu, Korea, Republic of
3 The Water and Salt Research Center, University of Aarhus, Aarhus, Denmark
4 Aarhus, Denmark; The Water and Salt Research Center, University of Aarhus, Aarhus, Denmark
* To whom correspondence should be addressed. E-mail: thkwon{at}knu.ac.kr.
Vasopressin and angiotensin II (AngII) play a major role in the renal water and sodium reabsorption. We demonstrated that AngII AT1 receptor blockade decreases dDAVP-induced water reabsorption and AQP2 levels in rats, suggesting cross-talk between these two peptide hormones (Am J Physiol Renal Physiol, 2005). To directly address this, primary cultured IMCD cells from male Sprague-Dawley rats were treated with 1) vehicle, 2) AngII, 3) AngII+AT1 receptor blocker (candesartan), 4) dDAVP, 5) AngII+dDAVP, or 6) AngII+dDAVP+candesartan for 15 min. Immunofluorescence microscopy revealed that AngII 10-8M or dDAVP 10-11M treatment (protocol 1) was associated with increased AQP2 labeling of the plasma membrane and decreased cytoplasmic labeling, respectively. cAMP levels increased significantly in response to AngII 10-8M treatment and were potentiated by dDAVP co-treatment (10-11M). Consistent with this, immunoblotting revealed that phosphorylated AQP2 expression was significantly increased by the co-treatment. The AngII-induced AQP2 targeting was blocked by candesartan (10-5M). In protocol 2, treatment with lower concentration of dDAVP (10-12M) or AngII (10-9M) was associated with unchanged subcellular AQP2 distribution, whereas co-treatment with dDAVP (10-12M) and AngII (10-9M) enhanced AQP2 targeting. This effect was inhibited by candesartan (10-5M) co-treatment. AngII-induced cAMP accumulation and AQP2 targeting were inhibited by co-treatment of PKC inhibition. In conclusion, AngII plays a role in the regulation of AQP2 targeting to the plasma membrane in IMCD cells through AT1 receptor activation and potentiates the effect of dDAVP on AQP2 plasma membrane targeting.
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