Chemotransduction in the carotid body : K+ current modulated by PO2 in type I chemoreceptor cells

The ionic currents of carotid body type I cells and their possible involvement in the detection of oxygen tension (Po2) in arterial blood are unknown. The electrical properties of these cells were studied with the whole-cell patch clamp technique, and the hypothesis that ionic conductances can be al...

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Bibliographic Details
Published in:Science (American Association for the Advancement of Science) 1988-07, Vol.241 (4865), p.580-582
Main Authors: LOPEZ-BARNEO, J, LOPEZ-LOPEZ, J. R, URENA, J, GONZALEZ, C
Format: Article
Language:English
Subjects:
Animals
Biological and medical sciences
Blood
Calcium - physiology
Carotid Body - physiology
Cells, Cultured
Chemoreceptor Cells - physiology
Electric Conductivity
Fundamental and applied biological sciences. Psychology
In Vitro Techniques
Ion Channels - physiology
Medical research
Membrane Potentials
Minerals
Oxygen
Oxygen - blood
Potassium - physiology
Rabbits
Sodium - physiology
Somesthesis and somesthetic pathways (proprioception, exteroception, nociception)
interoception
electrolocation. Sensory receptors
Vertebrates: nervous system and sense organs
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Summary:The ionic currents of carotid body type I cells and their possible involvement in the detection of oxygen tension (Po2) in arterial blood are unknown. The electrical properties of these cells were studied with the whole-cell patch clamp technique, and the hypothesis that ionic conductances can be altered by changes in PO2 was tested. The results show that type I cells have voltage-dependent sodium, calcium, and potassium channels. Sodium and calcium currents were unaffected by a decrease in PO2 from 150 to 10 millimeters of mercury, whereas, with the same experimental protocol, potassium currents were reversibly reduced by 25 to 50 percent. The effect of hypoxia was independent of internal adenosine triphosphate and calcium. Thus, ionic conductances, and particularly the O2-sensitive potassium current, play a key role in the transduction mechanism of arterial chemoreceptors.
ISSN:0036-8075
1095-9203
DOI:10.1126/science.2456613