Molecular Mechanisms for the Regulation of Water Transport in Amphibian Epithelia by Antidiuretic Hormone
| Title: | Molecular Mechanisms for the Regulation of Water Transport in Amphibian Epithelia by Antidiuretic Hormone |
|---|---|
| Authors: | Harris, H. William; Jo, Inho |
| Publisher: | Kidney International |
| Date Published: | October 01, 1995 |
| Reference Number: | 263 |
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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)
The ability to regulate water was aided by the ability to synthesize and use antidiuretic hormone (ADH). When amphibians are in the water, ADH plays no role in maintaining their water balance. But when they are out of water, ADH reduces body water loss by decreasing the amount of fluid that flows through the glomeri, the filters that form part of the nephron, the main working unit of the kidney. Also, ADH increases the amount of water that amphibians can reabsorb through their skin and urinary bladder. The amphibians can then soak up water through their skin and from their urinary bladder.
ADH accomplishes this by inducing molecular structures called water channels (WCs) to insert themselves into the apical membrane of the granular cells of the amphibian skin and bladder. (If you think of the cell as an upright rectangle whose perimeter is the membrane, the segment of the membrane that covers the bottom and sides is called the basolateral membrane. The segment that covers the top is the apical membrane.) WCs are proteins that act as channels through which water can flow across cell membranes.
When the WCs are not inserted in the apical membrane, very little water can pass through. In this state the apical membrane is actually the major barrier to tissue water flow. But when the WCs insert themselves into the apical membrane it becomes very water permeable and becomes the major gate through which water is absorbed.
In the toad urinary bladder the WC sits inside the granular cells within little sacs called vesicles. These WC vesicles (WCVs) carry the WCs to the apical membrane and fuse with it, allowing the WCs to insert themselves into the membranes. WCVs also retrieve the WCs from the apical membrane, first sequestering in tubular and early multivesicular body (MVB) endosomes. (Endosomes are vesicles that have lost their coat of a protein called clathrin upon returning inside the cell from the cell surface.) These endosomes are not acidic and do not dissolve the WCs within them. Later, the endosomes travel to late MVBs, and researchers examining the endosomes there found no WCs and an acidic content. This indicates that the WCs are dissolved at this stage. It is currently unclear whether WCVs with intact and functional WCs recycle back and forth to the apical membrane one or more times before being dissolved.
The human red blood cell contains a WC known as aquaporin-CHIP (AQP-CHIP). This WC is found in two parts of the kidney nephron: the proximal tubule (PT) and the thin descending limb of Henle (TDL). It is generally believed that AQP-CHIP is not regulated by ADH. That is, it does not insert itself in the cell membrane upon receiving a signal from ADH. Rather, AQP-CHIP resides permanently in the cell membrane and functions whether or not ADH is present. Thus, there may be aquaporins (AQPs) that operate constitutively (i.e. independently of hormone-regulation) and AQPs that are regulated by ADH. In both cases AQPs increase the level of cell membrane water permeability.
The body can regulate AQPs in both a short-term and long-term manner. In the short-term it uses ADH to send AQPs to the cell surface. This short-term increase in AQPs is rapid and can be rapidly reversed. The body increases AQPs in a long-term manner when it synthesizes more AQPs than normal in response to dehydration. Both anurans (frogs and toads) and mammals increase the amount of AQPs in their bodies after a period of dehydration. This long-term upleveling of AQPs accrues over time and takes time to reverse itself.