Calcimimetic acts on enteric neuronal CaSR to reverse cholera toxin-induced intestinal electrolyte secretion
| Autor: | Megan E. McIntyre, Sam X. Cheng, Ekaterina Petrova, Lieqi Tang, Lingli Jiang |
|---|---|
| Jazyk: | angličtina |
| Rok vydání: | 2018 |
| Předmět: |
0301 basic medicine
Male Cholera Toxin Calcimimetic Colon lcsh:Medicine Cell Communication Tetrodotoxin Pharmacology medicine.disease_cause Article Enteric Nervous System 03 medical and health sciences Electrolytes Mice Intestinal mucosa Phenethylamines medicine Animals Secretion Intestinal Mucosa Receptor lcsh:Science Evoked Potentials Mice Knockout Multidisciplinary Ussing chamber Propylamines Chemistry Cholera toxin lcsh:R Lidocaine Intestinal epithelium 3. Good health Mice Inbred C57BL 030104 developmental biology Enteric nervous system lcsh:Q Female Receptors Calcium-Sensing |
| Zdroj: | Scientific Reports Scientific Reports, Vol 8, Iss 1, Pp 1-10 (2018) |
| ISSN: | 2045-2322 |
| Popis: | Treatment of acute secretory diarrheal illnesses remains a global challenge. Enterotoxins produce secretion through direct epithelial action and indirectly by activating enteric nervous system (ENS). Using a microperfused colonic crypt technique, we have previously shown that R568, a calcimimetic that activates the calcium-sensing receptor (CaSR), can act on intestinal epithelium and reverse cholera toxin-induced fluid secretion. In the present study, using the Ussing chamber technique in conjunction with a tissue-specific knockout approach, we show that the effects of cholera toxin and CaSR agonists on electrolyte secretion by the intestine can also be attributed to opposing actions of the toxin and CaSR on the activity of the ENS. Our results suggest that targeting intestinal CaSR might represent a previously undescribed new approach for treating secretory diarrheal diseases and other conditions with ENS over-activation. |
| Databáze: | OpenAIRE |
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