Vasopressin-Independent Renal Urinary Concentration: Increased rBSC1 and Enhanced Countercurrent Multiplication
|Title:||Vasopressin-Independent Renal Urinary Concentration: Increased rBSC1 and Enhanced Countercurrent Multiplication|
|Authors:||Michimata, Mari; Mizukami, Kazuhiko; Suzuki, Michiko; Kazama, Itsuro; Nakamura, Yohsuke; Suzuki, Katsuya; Yanagisawa, Teruyuki; Imai, Yutaka; Sasaki, Sei; Matsubara, MD, PhD, Mitsunobu|
|Date Published:||September 01, 2003|
This translation by the NDI Foundation is to assist the lay reader. To provide a clear, accessible interpretation of the original article, we eliminated or simplified some technical detail and complicated scientific language. We concentrated our translation on those aspects of the article dealing directly with NDI. The NDI Foundation thanks the researchers for their work toward understanding and more effectively treating this disorder.
© Copyright NDI Foundation 2007 (JC)
Michimata, et al., knew that there is in Brattleboro rats (BB) a close association between the expression of the sodium transporter, rat bumetanide sensitive co-transporter (rBSC) in the thick ascending limb of Henle (a specific portion of the loops of Henle) and urinary concentration. They investigated the effects on rBSC1 that occurred when rats were subjected to dehydration. rBSC1 cotransports sodium chloride (NaCl) into the kidney’s inner tissue, which creates favorable osmotic conditions for urine concentration. It works in harmony with aquaporin 2 (AQP2) and urea transporters to establish final conditions for urine concentration. AQP2 availability is determined by AVP.
BB rats lack the ability to synthesize AVP, thus they do not concentrate urine well. However, when BB rats are blocked access to drinking water and become dehydrated, they show a capacity to concentrate urine. This may indicate that rBSC1 can be expressed by a biological mechanism other than AVP stimuli.
The research team restricted BB rats from water consumption for 4 hours. This resulted in a 5% reduction in the rats' body weight. Even under these conditions, no AVP was detectable in the rats. Still, they were able to concentrate their urine. The rats increased the amounts of sodium and urea in the kidney medulla and reduced the amount of sodium they excreted in their urine. The amount of rBSC1 in the rats increased, but not the amount of AQP2. This indicates that AQP2 expression had little influence on the urinary concentration in dehydrated BB rats. The team’s data indicates that it is rBSC1 expression that initiates countercurrent multiplication for the rats' urinary concentration mechanism.
When the researchers injected the rats with a synthetic analogue of AVP called dDAVP, they observed a significant increase in the amount of AQP2 generated in the rats. When they treated the rats with an AQP2 blocker and again injected them with dDAVP, the rats were able to concentrate urine even less well than normal. However, when they were dehydrated, they were able to concentrate urine and increase the amount of rBSC1 in them. Thus, the team’s research indicates that there exists in BB rats different mechanisms for rBSC1 expression. One needs AVP and another does not. Both may independently be involved in urinary concentration.
The researchers now know rBSC1 plays a significant part in urinary concentration and suspect it promotes countercurrent multiplication. The presence of an AVP-independent mechanism for urine concentration is exciting, and the researchers plan to investigate further.