Ca2+-activated K+-channels from isolated type I carotid body cells of the neonatal rat

C. N. Wyatt; C. Peers

doi:10.1007/978-1-4615-2572-1_18

Ca²⁺-activated K⁺-channels from isolated type I carotid body cells of the neonatal rat

C. N. Wyatt, C. Peers

Neuroscience, Cell Biology, and Physiology (NCBP)

Research output: Chapter in Book/Report/Conference proceeding › Conference contribution

Abstract

Over the past five years, the patch-clamp technique has been applied to type I cells isolated from carotid bodies of rats and rabbits (e.g. Duchen et al., 1988; Lopez-Barneo et al., 1988; Delpiano & Hescheler, 1989; Peers, 1990a; Stea & Nurse, 1991). Our previous studies, using type I cells from rats (approximately 10 days old) have shown that whole-cell K+ currents can be subdivided into two types; a Ca2+-activated, charybdotoxin-sensitive current, IKCa, and a Ca2+-independent, voltage-gated current, IKV (Peers, 1990a,b). Of these, IKCa can be inhibited by chemostimuli such as hypoxia (Peers, 1990b), acidity (Peers, 1990a; Peers and Green, 1991) or the respiratory stimulant doxapram (Peers, 1991). Here, we describe the properties of the single Ca2+-activated K+ channels which underlie the macroscopic IKCa, and show that doxapram can inhibit this channel without the involvement of a second messenger system.

Original language	English
Title of host publication	Arterial Chemoreceptors
Subtitle of host publication	Cell to System
Editors	Ronan G. O'Regan, Philip Nolan, Daniel S. McQueen, David J. Paterson
Publisher	Springer New York
Pages	159-161
Number of pages	3
Volume	360
ISBN (Electronic)	978-1-4615-2572-1
ISBN (Print)	978-0-306-44824-9, 978-1-4613-6099-5
DOIs	https://doi.org/10.1007/978-1-4615-2572-1_18
State	Published - 1994
Event	12th International Meeting on Arterial Chemoreception - Dublin, Ireland Duration: Aug 1 1993 → Aug 1 1993 Conference number: 19

Publication series

Name	Advances in Experimental Medicine and Biology
ISSN (Print)	0065-2598

Conference

Conference	12th International Meeting on Arterial Chemoreception
Country/Territory	Ireland
City	Dublin
Period	8/1/93 → 8/1/93

ASJC Scopus Subject Areas

General Biochemistry,Genetics and Molecular Biology

Keywords

Potassium channels
Physiological effects of calcium
Carotid body/physiology

Disciplines

Molecular and Cellular Neuroscience
Medical Neurobiology

Access to Document

10.1007/978-1-4615-2572-1_18

Cite this

Ca²⁺-activated K⁺-channels from isolated type I carotid body cells of the neonatal rat. / Wyatt, C. N.; Peers, C.
Arterial Chemoreceptors : Cell to System. ed. / Ronan G. O'Regan; Philip Nolan; Daniel S. McQueen; David J. Paterson. Vol. 360 Springer New York, 1994. p. 159-161 (Advances in Experimental Medicine and Biology).

Research output: Chapter in Book/Report/Conference proceeding › Conference contribution

Wyatt, CN & Peers, C 1994, Ca²⁺-activated K⁺-channels from isolated type I carotid body cells of the neonatal rat. in RG O'Regan, P Nolan, DS McQueen & DJ Paterson (eds), Arterial Chemoreceptors : Cell to System. vol. 360, Advances in Experimental Medicine and Biology, Springer New York, pp. 159-161, 12th International Meeting on Arterial Chemoreception, Dublin, Ireland, 8/1/93. https://doi.org/10.1007/978-1-4615-2572-1_18

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AB - Over the past five years, the patch-clamp technique has been applied to type I cells isolated from carotid bodies of rats and rabbits (e.g. Duchen et al., 1988; Lopez-Barneo et al., 1988; Delpiano & Hescheler, 1989; Peers, 1990a; Stea & Nurse, 1991). Our previous studies, using type I cells from rats (approximately 10 days old) have shown that whole-cell K+ currents can be subdivided into two types; a Ca2+-activated, charybdotoxin-sensitive current, IKCa, and a Ca2+-independent, voltage-gated current, IKV (Peers, 1990a,b). Of these, IKCa can be inhibited by chemostimuli such as hypoxia (Peers, 1990b), acidity (Peers, 1990a; Peers and Green, 1991) or the respiratory stimulant doxapram (Peers, 1991). Here, we describe the properties of the single Ca2+-activated K+ channels which underlie the macroscopic IKCa, and show that doxapram can inhibit this channel without the involvement of a second messenger system.

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