RT info:eu-repo/semantics/article
T1 Time course of K+ current inhibition by low oxygen in chemoreceptor cells of adult rabbit carotid body. Effects of carbon monoxide
A1 López López, José Ramón
A1 González, Constancio
K1 Células - Receptores
K1 Cuerpo carotídeo
K1 Cells - Receptors
K1 Carotic body
AB Carotid body (CB) chemoreceptors respond to a decreasein arterial blood pOz with an increase in actionpotential frequency in the sensory fibers innervating theorgan, the response developing in a few seconds [l].Chemoreceptor cells of the CB are the Oz sensing structures,releasing neurotransmitters in proportion to thepOz decrease and producing an electrical discharge ofparallel intensity in the sensory nerve fibers of the carotidsinus nerve [2,3]. Recently, it has been shown thatchemoreceptor cells possess an O,-sensitive K’ currentthat is reversibly inhibited by decreasing pOz in thebathing solution. The suggestion was made that thisinhibition can lead to cell depolarization and activationof voltage-dependent Ca” channels [4,5]; the entry ofCa”+ through these channels, that are dihydropyridinesensitive,would trigger the release of neurotransmitters[6,7]. To accept this sequence, the inhibition of the K’current must precede the activation of the sensory nervedischarges [8], that is, the inhibition mus: developwithin the initial 3 s after lowering pOz, the time elapsingbetween a decrease in arterial pO1! and the increasein the carotid sinus nerve action potential frequency [l].On the other hand, the suggestion has been made thatthe O?-sensor in chemoreceptor cells should be a hemoglobin-like hemoprotein, but no direct evidence tosupport this suggestion is available [l]. The presentstudy compares the time course of the inhibition of theK’ current by low pO1 and that of Na” current inhibitionby TTX, which is known to occur in a few hundredms [SJ. I: is shown that the former inhibition is faster.It is also shown that carbon monoxide, a very inert gasthat in biological systems only reacts with hemoproteins,prevents the low PO,-induced inhibition ofchemorcceptor cells E;” current.
PB Elsevier
SN 0014-5793
YR 1992
FD 1992
LK http://uvadoc.uva.es/handle/10324/6821
UL http://uvadoc.uva.es/handle/10324/6821
LA eng
NO FEBS Letters, 1992, vol. 299, n. 3. p. 251-254
NO Producción Científica
DS UVaDOC
RD 22-dic-2024