2002 Global Researcher Conference Proceeding
April 26 - 28, 2002
| Conference: | 2002 Global Researcher Conference |
|---|---|
| Title: | Expressional alteration of sodium transporter in the thick ascending limb of Henle and urinary concentration |
| Authors: | Matsubara, MD, PhD, Mitsunobu; Michimata, Mari; Mizukami, Kazuhiko; Araki, Tsutomu; Kazama, Itsuro; Suzuki, Michiko; Sasaki, Sei |
| Institutions: | Tohoku University Graduate School of Medicine, Tohoku University Graduate School of Medicine and Pharmaceutical Science, Tohoku University, Tokyo Medical & Dental University |
Sodium transporter in thick ascending limb of Henle, rBSC1, supplies energy for counter current multiplier. The expressional alteration of rBSC1 has been described in various systemic or renal diseases. In the present study we assessed the association between rBSC1 expression and urinary concentration. To this end, rats model for dehydration, congestive heart failure (CHF), unilateral nephrectomy (UNX), chronic renal failure by 5/6 nephrectomy (CRF), kidney isograft, and congenital defect of vasopressin excretion (Brattleboro; BB rats) were examined and analyzed together. Enhanced expression was noted in dehydrated rats, CHF, and UNX, indicating that rBSC1 is increased in the conditions in which retention of body fluid is promoted or compensatory tubular function is required. On the contrary, insufficient rBSC1 expression was observed in kidney isograft and CRF. These rats demonstrated limited ability of urinary concentration. In these models, dehydration, CHF, UNX, kidney isograft, and CRF, the expression of apical water channel in collecting duct (AQP2) showed the same trend as observed in rBSC1 expression. These results indicate rBSC1 expression is closely associated with urinary concentration and also with vasopressin stimuli. However, in BB rats, urinary concentration and increased rBSC1, but no alteration of AQP2, were observed, when the rats were dehydrated. Therefore expressional regulation of rBSC1 is considered to be involved in both vasopressin-dependent and independent mechanisms of urinary concentration.



