{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,29]],"date-time":"2026-09-29T00:38:00Z","timestamp":1790642280433,"version":"4.1.0"},"reference-count":43,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2006,8,8]],"date-time":"2006-08-08T00:00:00Z","timestamp":1154995200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["The Journal of Physiology"],"published-print":{"date-parts":[[2006,8,15]]},"abstract":"<jats:p>Angiotensin II (Ang II) plays an important role in the enhanced chemoreflex function that occurs in congestive heart failure (CHF), but the mechanism of this effect within the carotid body (CB) is not known. We investigated the sensitivity of Ca<jats:sup>2+<\/jats:sup>\u2010independent, voltage\u2010gated K<jats:sup>+<\/jats:sup> (Kv) channels to hypoxia in CB glomus cells from CHF rabbits, and whether endogenous angiotensin II (Ang II) modulates this action. Using the conventional whole\u2010cell patch clamp technique, we found that Kv currents (<jats:italic>I<\/jats:italic><jats:sub>K<\/jats:sub>) under normoxic conditions were blunted in the CB glomus cells from CHF rabbits compared with sham rabbits. In addition, the inhibition of <jats:italic>I<\/jats:italic><jats:sub>K<\/jats:sub> and the decrease of resting membrane potential (RMP) induced by hypoxia were greater in CHF <jats:italic>versus<\/jats:italic> sham glomus cells. Ang II, at 100 p<jats:sc>m<\/jats:sc>, had no direct effect on <jats:italic>I<\/jats:italic><jats:sub>K<\/jats:sub> at constant normoxic <jats:italic>P<\/jats:italic><jats:sub>O2<\/jats:sub>, but increased the sensitivity of <jats:italic>I<\/jats:italic><jats:sub>K<\/jats:sub> and RMP to hypoxia in sham glomus cells. In CHF glomus cells, an AT1 receptor (AT<jats:sub>1<\/jats:sub>R) antagonist, L\u2010158 809 (1 \u03bc<jats:sc>m<\/jats:sc>), alone did not affect <jats:italic>I<\/jats:italic><jats:sub>K<\/jats:sub> at normoxia, but it decreased the sensitivity of <jats:italic>I<\/jats:italic><jats:sub>K<\/jats:sub> and RMP to hypoxia. At higher concentrations, Ang II dose dependently (0.1\u2013100 n<jats:sc>m<\/jats:sc>) reduced <jats:italic>I<\/jats:italic><jats:sub>K<\/jats:sub> under constant normoxic conditions in sham and CHF glomus cells, with threshold concentrations of about 900 and 600 p<jats:sc>m<\/jats:sc>, respectively. Immunocytochemical and Western blot assessments demonstrated the down\u2010expression of Kv3.4 but not Kv4.3 channels in CHF glomus cells. These results indicate that: (1) Ang II\/AT<jats:sub>1<\/jats:sub>R signalling increases the sensitivity of Kv channels to hypoxia in CB glomus cells from CHF rabbits; (2) high concentrations of Ang II (&gt; 1 n<jats:sc>m<\/jats:sc>) directly inhibit <jats:italic>I<\/jats:italic><jats:sub>K<\/jats:sub> in CB glomus cells from sham and CHF rabbits; (3) changes in Kv channel protein expression (Kv3.4 <jats:italic>versus<\/jats:italic> Kv4.3) in the CB glomus cell may contribute to the suppression of <jats:italic>I<\/jats:italic><jats:sub>K<\/jats:sub> and enhanced sensitivity of <jats:italic>I<\/jats:italic><jats:sub>K<\/jats:sub> to hypoxia in CHF.<\/jats:p>","DOI":"10.1113\/jphysiol.2006.110700","type":"journal-article","created":{"date-parts":[[2006,6,16]],"date-time":"2006-06-16T00:56:36Z","timestamp":1150419396000},"page":"215-227","source":"Crossref","is-referenced-by-count":65,"title":["Enhanced sensitivity of Kv channels to hypoxia in the rabbit carotid body in heart failure: 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