Impaired osmotic sensation in mice lacking TRPV4
Impaired osmotic sensation in mice lacking TRPV4
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DOI：
10.1152/ajpcell.00559.2002
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发表时间：
2003-07-01
影响因子：
5.5
通讯作者：
Suzuki, M
中科院分区：
文献类型：
--
作者：
Mizuno, A;Matsumoto, N;Suzuki, M
Ca 2+渗透性阳离子通道TRPV 4是位于室周器官中的Trp家族的一部分，通过细胞肿胀激活。为了研究TRPV 4在渗透感觉中的作用，我们破坏了小鼠的TRPV 4基因，并检查了对渗透代谢的影响。小鼠TRPV 4基因的破坏不影响饮水行为或血清渗透压。然而，短期盐摄入似乎会损害瞬时自由水清除率。TRPV 4-/-小鼠血清精氨酸加压素（AVP）水平在正常条件下无显著变化，但在刺激条件下显著升高。用分级的高渗透压浓度孵育脑切片表明TRPV 4-/-小鼠中AVP分泌的过度反应。因此，大脑中的TRPV 4可能会向AVP分泌传递负信号，类似于通过压力调节系统的抑制性传递。因此，在血清渗透压的调节中，TRPV 4是一种溶胀激活的通道，似乎在向低渗透压的逆转中发挥作用。
The Ca2+-permeable cation channel TRPV4, which is part of the Trp family located in the circumventricular organs, is activated by cell swelling. To investigate the role of TRPV4 in osmotic sensation, we disrupted the TRPV4 gene in mice and examined the effect on osmotic metabolism. Disruption of the mouse TRPV4 gene did not influence either water intake behavior or serum osmolality. Short-term salt ingestion, however, seemed to impair the transient free water clearance. The level of serum arginine vasopressin (AVP) of TRPV4-/- mice was not significantly changed under normal conditions but was significantly increased under stimulated conditions. Incubation of brain slices with graded hyperosmolality suggested an exaggerated response of AVP secretion in TRPV4-/- mice. Thus TRPV4 in the brain may transmit a negative signal to AVP secretion similar to an inhibitory pass through the baroregulatory system. Thus, in the regulation of serum osmolality, TRPV4 is a swell-activated channel that appears to play a role in reversion toward hyposmolality.