Angaben zur Quelle [Bearbeiten]
| Titel | Calcium |
| Jahr | 2005 |
| Anmerkung | PPT file properties: "Last modified: 15/03/2005". Much of the text and many of the illustrations are from book chapter "Approach to Hypercalcemia", David Goltzman, 2000-2016 http://www.endotext.org/chapter/approach-to-hypercalcemia/?singlepage=true also found at Favus & Goltzman 2008 |
| URL | http://www.med.muni.cz/patfyz/powerpnt/new/Calcium2005.ppt |
Literaturverz. |
no |
| Fußnoten | no |
| Fragmente | 1 |
| [1.] Dsa/Fragment 041 04 - Diskussion Zuletzt bearbeitet: 2016-08-07 12:09:47 WiseWoman | Calcium 2005, Dsa, Fragment, Gesichtet, SMWFragment, Schutzlevel sysop, Verschleierung |
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| Untersuchte Arbeit: Seite: 41, Zeilen: 4-6, 9-27 |
Quelle: Calcium 2005 Seite(n): 19, 21, 22, 23, Zeilen: Slides 19: 2ff; 21: 1ff; 22: 1ff; 23: 1ff |
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| PTH has little effect on modulating calcium fluxes in the proximal tubule where 65% of the filtered calcium is reabsorbed, by being coupled to the transport of solutes such as sodium and water. [...] About 20% of filtered calcium is reabsorbed in the cortical thick ascending limb of the loop of Henle (CTAL) and 15% in the distal convoluted tubule (DCT). Here PTH also binds to the PTHR and again by a cyclic AMP-mediated mechanism, enhances calcium reabsorption. In the CTAL, this appears to occur by increasing the activity of the Na+-K+-2Cl- cotransporter that drives NaCl reabsorption and also stimulates paracellular calcium and magnesium reabsorption.
The extracellular calcium sensor is also resident in the CTAL and can respond to increased ECF calcium by activating phospholipase A2, reducing the activity of the Na+-K+-2Cl- cotransporter and of an apical K+ channel, and diminishing paracellular calcium and magnesium reabsorption. Consequently raised ECF calcium antagonizes the effect of PTH in this region of the kidney and ECF calcium can regulate its own homeostasis. In the DCT, PTH can also influence transcellular calcium transport. This is a multistep process involving transfer of luminal Ca2+ into the renal tubule cell via the transient receptor potential channel (TRPV5) or ECaC (epithelial calcium channel), translocation of Ca2+ across the cell from apical to basolateral surface a process involving proteins such as calbindin- D28K and finally active extrusion of Ca2+ from the cell into the blood via a Na+-Ca2+ exchanger, designated NCX1 and the Ca2+-ATPase pump. PTH markedly stimulates Ca2+ reabsorption in the DCT primarily by augmenting NCX1 activity via a cyclic AMP-mediated mechanism. |
[slide 19]
PTH has little effect on modulating calcium fluxes in the proximal tubule where 65% of the filtered calcium is reabsorbed, coupled to the bulk transport of solutes such as sodium and water. [slide 21] About 20% of filtered calcium is reabsorbed in the cortical thick ascending limb of the loop of Henle (CTAL) and 15% in the distal convoluted tubule (DCT) and it is here that PTH also binds to the PTHR and again by a cyclic AMP-mediated mechanism, enhances calcium reabsorption. In the CTAL, at least, this appears to occur by increasing the activity of the Na/K/2Cl cotransporter that drives NaCl reabsorption and also stimulates paracellular calcium and magnesium reabsorption. [slide 22] The CaSR is also resident in the CTAL and can respond to an increased ECF calcium by activating phospholipase A2, reducing the activity of the Na/K/2Cl cotransporter and of an apical K channel, and diminishing paracellular calcium and magnesium reabsorption. Consequently a raised ECF calcium antagonizes the effect of PTH in this nephron segment and ECF calcium can in fact participate in this way in the regulation of its own homeostasis. [slide 23] In the distal convoluted tubule (DCT), PTH can also influence transcellular calcium transport. This is a multistep process involving
PTH markedly stimulates Ca2+ reabsorption in the DCT primarily by augmenting NCX1 activity via a cyclic AMP-mediated mechanism |
No source is given for this passage. The source is probably not the PowerPoint slide set but the online textbook that was first published in 2000. However, the book is constantly updated and not archived on the Internet Archive, so this is the only source. Both PowerPoint and textbook do not use superscripts. |
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