Abstract
Central to the maintenance of calcium homeostasis is the regulated reabsorption of calcium along the nephron. To this end, parathyroid hormone (PTH) is released from the parathyroid gland in response to lowered plasma calcium levels. This hormone acts through the PTH 1 receptor along the nephron to increase urinary phosphate excretion and decrease urinary calcium excretion. In the proximal tubule, PTH inhibits phosphate reabsorption by reducing the abundance of sodium phosphate cotransporters in the apical membrane. PTH likely decreases calcium reabsorption from the proximal tubule, by reducing the reabsorption of sodium, an event necessary for the paracellular movement of calcium across this segment. In the thick ascending limb (TAL), PTH increases calcium permeability and may increase the electrical driving force thereby increasing calcium reabsorption in the TAL. Finally, in the distal convolution, PTH acts to increase transcellular calcium reabsorption by increasing the activity and abundance of the apically expressed calcium channel TRPV5.
| Originalsprog | Engelsk |
|---|---|
| Artikelnummer | e13959 |
| Tidsskrift | Acta Physiologica |
| Vol/bind | 238 |
| Udgave nummer | 1 |
| Antal sider | 16 |
| ISSN | 1748-1708 |
| DOI | |
| Status | Udgivet - maj 2023 |
Bibliografisk note
Funding Information:Research in the R.T.A. laboratory is funded by grants from the Women and Children's Health Research Institute, which is supported by the Stollery Children's Hospital Foundation, the Canadian Institutes of Health Research, the Kidney Foundation of Canada, and the National Sciences and Engineering Research Council of Canada. R.T.A. is a Stollery Science Laboratory Distinguished Researcher and the Canada Research Chair in Epithelial Transport Physiology. The lab of H. Dimke is funded by the Novo Nordisk Foundation, the Carlsberg Foundation and Independent Research Fund Denmark.