Ca(2+)-activated K+ channels in isolated type I cells of the neonatal rat carotid body
1. Ca(2+)-activated K+ (K+Ca) channels in neonatal rat type I carotid body cells were studied using single channel patch clamp techniques. In outside-out patches, using symmetrical 120 mM [K+] solutions, channels were observed with a slope conductance of 190 pS and a reversal potential of 0 mV. Redu...
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Veröffentlicht in: | The Journal of physiology 1995-03, Vol.483 (Pt 3), p.559-565 |
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Sprache: | eng |
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Zusammenfassung: | 1. Ca(2+)-activated K+ (K+Ca) channels in neonatal rat type I carotid body cells were studied using single channel patch clamp
techniques. In outside-out patches, using symmetrical 120 mM [K+] solutions, channels were observed with a slope conductance
of 190 pS and a reversal potential of 0 mV. Reducing [K+]o to 5 mM shifted the reversal potential as expected for a K(+)-selective
channel. 2. With 100 nM Ca2+ bathing the cytosolic aspect of patches, channel activity (number of active channels in a patch
x open probability, NPo) increased with depolarization. NPo also increased with increasing 'cytosolic' [Ca2+] at a fixed membrane
potential (0 mV). Using outside-out patches, bath application of 20 or 100 nM charybdotoxin reduced NPo by > 85%. These data
indicate the presence of K+Ca channels in type I cells. 3. At 0 mV, using solutions of identical composition (1 microM Ca2+
bathing the cytosolic aspect of the channels), NPo was higher in outside-out patches than in inside-out patches. NPo was greatest
in recordings using the perforated-vesicle technique. 4. Hypoxia and anoxia were without effect on K+Ca channels in outside-out
patches, but caused significant, reversible reductions of NPo in channels recorded in perforated vesicles. 5. The whole-cell
perforated-patch technique was used to record membrane potential at 35-37 degrees C. Hypoxia, anoxia and charybdotoxin all
depolarized type I cells. 6. Our results suggest an important role for K+Ca channels in type I carotid body cells, and their
activity in relation to a model for chemotransduction is discussed. |
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ISSN: | 0022-3751 1469-7793 |
DOI: | 10.1113/jphysiol.1995.sp020606 |