Abstract |
Charybdotoxin ( ChTX), a venom protein, suppresses Ca2+-activated K+ (K+(Ca)) currents in the glomus cell of neonatal rat carotid body. If it works similarly for cat carotid body chemoreceptors, charybdotoxin is expected to stimulate the chemosensory discharge during normoxia, and particularly hypoxia and hypercapnia. We studied the effects of charybdotoxin (20-40 nM) in vitro (perfused/superfused) on the cat carotid chemosensory discharge, and simultaneously tissue PO2 (PtiO2), as a measure of positive control. ChTX (20 nM) only increased PtiO2 and decreased carotid chemosensory discharge during hypoxia, indicating vasodilation. We conclude that K+(Ca) channels do not appear to play a significant role in chemotransduction in the cat carotid body.
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Authors | S Osanai, D G Buerk, A Mokashi, D K Chugh, S Lahiri |
Journal | Brain research
(Brain Res)
Vol. 747
Issue 2
Pg. 324-7
(Feb 07 1997)
ISSN: 0006-8993 [Print] Netherlands |
PMID | 9046009
(Publication Type: Journal Article, Research Support, U.S. Gov't, P.H.S.)
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Chemical References |
- Potassium Channels
- Charybdotoxin
- Oxygen
- Calcium
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Topics |
- Animals
- Calcium
(pharmacology)
- Carotid Body
(drug effects)
- Cats
- Cell Hypoxia
(drug effects)
- Charybdotoxin
(pharmacology)
- Chemoreceptor Cells
(drug effects)
- Female
- Hypercapnia
(metabolism)
- In Vitro Techniques
- Linear Models
- Male
- Oxygen
(metabolism)
- Partial Pressure
- Potassium Channels
(drug effects)
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