<?xml version="1.0" encoding="UTF-8"?><?xml-stylesheet type="text/xsl" href="static/style.xsl"?><OAI-PMH xmlns="http://www.openarchives.org/OAI/2.0/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.openarchives.org/OAI/2.0/ http://www.openarchives.org/OAI/2.0/OAI-PMH.xsd"><responseDate>2026-04-14T21:04:29Z</responseDate><request verb="GetRecord" identifier="oai:uvadoc.uva.es:10324/7031" metadataPrefix="mods">https://uvadoc.uva.es/oai/request</request><GetRecord><record><header><identifier>oai:uvadoc.uva.es:10324/7031</identifier><datestamp>2025-03-03T10:28:37Z</datestamp><setSpec>com_10324_32522</setSpec><setSpec>com_10324_952</setSpec><setSpec>com_10324_894</setSpec><setSpec>com_10324_43677</setSpec><setSpec>com_10324_954</setSpec><setSpec>com_10324_1134</setSpec><setSpec>com_10324_931</setSpec><setSpec>col_10324_32523</setSpec><setSpec>col_10324_43678</setSpec><setSpec>col_10324_1213</setSpec></header><metadata><mods:mods xmlns:mods="http://www.loc.gov/mods/v3" xmlns:doc="http://www.lyncode.com/xoai" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.loc.gov/mods/v3 http://www.loc.gov/standards/mods/v3/mods-3-1.xsd">
<mods:name>
<mods:namePart>López López, José Ramón</mods:namePart>
</mods:name>
<mods:name>
<mods:namePart>González Martínez, Constancio</mods:namePart>
</mods:name>
<mods:name>
<mods:namePart>Ureña, J.</mods:namePart>
</mods:name>
<mods:name>
<mods:namePart>López Barneo, José</mods:namePart>
</mods:name>
<mods:extension>
<mods:dateAvailable encoding="iso8601">2014-11-07T12:13:03Z</mods:dateAvailable>
</mods:extension>
<mods:extension>
<mods:dateAccessioned encoding="iso8601">2014-11-07T12:13:03Z</mods:dateAccessioned>
</mods:extension>
<mods:originInfo>
<mods:dateIssued encoding="iso8601">1989</mods:dateIssued>
</mods:originInfo>
<mods:identifier type="citation">Journal of General Phisiology, 1989, vol. 93, n. 5. p. 1001-1015</mods:identifier>
<mods:identifier type="issn">0022-1295</mods:identifier>
<mods:identifier type="uri">http://uvadoc.uva.es/handle/10324/7031</mods:identifier>
<mods:identifier type="doi">10.1085/jgp.93.5.1001</mods:identifier>
<mods:identifier type="publicationfirstpage">1001</mods:identifier>
<mods:identifier type="publicationlastpage">1015</mods:identifier>
<mods:identifier type="publicationtitle">Journal of General Phisiology</mods:identifier>
<mods:identifier type="publicationvolume">93</mods:identifier>
<mods:abstract>The hypothesis that changes in environmental 02 tension (pOi) could&#xd;
affect the ionic conductances of dissociated type I cells of the carotid body was&#xd;
tested. Cells were subjected to whole-cell patch clamp and ionic currents were&#xd;
recorded in a control solution with normal pO 2 (pO~ = 150 mmHg) and 3-5 min&#xd;
after exposure to the same solution with a lower pO,. Na and Ca currents were&#xd;
unaffected by lowering pO, to 10 mmHg, however, in all cells studied (n = 42)&#xd;
exposure to hypoxia produced a reversible reduction of the K current. In 14 cells&#xd;
exposed to a pO 2 of 10 mmHg peak K current amplitude decreased to 35 +_ 8% of&#xd;
the control value. The effect of low pO2 was independent of the internal Ca 2+&#xd;
concentration and was observed in the absence of internal exogenous nucleotides.&#xd;
Inhibition of K channel activity by hypoxia is a graded phenomenon and in the&#xd;
range between 70 and 120 mmHg, which includes normal pO, values in arterial&#xd;
blood, it is directly correlated with pO 2 levels. Low pO2 appeared to slow down the&#xd;
activation time course of the K current but deactivation kinetics seemed to be&#xd;
unaltered. Type I cells subjected to current clamp generate large Na- and Cadependent&#xd;
action potentials repetitively. Exposure to low pO~ produces a 4-10&#xd;
mV increase in the action potential amplitude and a faster depolarization rate of&#xd;
pacemaker potentials, which leads to an increase in the firing frequency. Repolarization&#xd;
rate of individual action potentials is, however, unaffected, or slightly&#xd;
increased. The selective inhibition of K channel activity by low pO, is a phenomenon&#xd;
without precedents in the literature that explains the chemoreceptive properties&#xd;
of type I cells. The nature of the interaction of molecular O, with the K channel&#xd;
protein is unknown, however, it is argued that a hemoglobin-like O, sensor,&#xd;
perhaps coupled to a G protein, could be involved.</mods:abstract>
<mods:language>
<mods:languageTerm>eng</mods:languageTerm>
</mods:language>
<mods:accessCondition type="useAndReproduction">info:eu-repo/semantics/openAccess</mods:accessCondition>
<mods:accessCondition type="useAndReproduction">© 1989 The Rockefeller University Press</mods:accessCondition>
<mods:subject>
<mods:topic>Neurofisiología</mods:topic>
</mods:subject>
<mods:subject>
<mods:topic>Neurophysiology</mods:topic>
</mods:subject>
<mods:titleInfo>
<mods:title>Low pO2 selectively inhibits K channel activity in chemoreceptor cells of the mammalian carotid body</mods:title>
</mods:titleInfo>
<mods:genre>info:eu-repo/semantics/article</mods:genre>
</mods:mods></metadata></record></GetRecord></OAI-PMH>