<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Zhao W</submitter><funding>National Natural Science Foundation of China</funding><pagination>e7111</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC6571133</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>7</volume><pubmed_abstract>&lt;h4>Background and objectives&lt;/h4>Hyperpolarization-activation cyclic nucleotide-gated (HCN) channels contribute to the effects of lidocaine. Capsazepine (CPZ), a competitive inhibitor of capsaicin of transient receptor potential vanilloid-1 channel, has also been found to inhibit HCN channel currents (&lt;i>I&lt;/i> &lt;sub>h&lt;/sub>). This study was designed to investigate whether CPZ could prolong durations of lidocaine in regional anesthesia.&lt;h4>Methods&lt;/h4>Mouse HCN1 and HCN2 channels were expressed in human embryonic kidney 293 (HEK 293) cells. The effect of CPZ on &lt;i>I&lt;/i> &lt;sub>h&lt;/sub> was measured by whole-cell patch-clamping recording. Sciatic nerve block model in mice was used for the study in vivo. The mice were randomly divided into seven groups, respectively, receiving lidocaine, CPZ, ZD</pubmed_abstract><journal>PeerJ</journal><pubmed_title>Capsazepine prolongation of the duration of lidocaine block of sensory transmission in mice may be mediated by modulation of HCN channel currents.</pubmed_title><pmcid>PMC6571133</pmcid><funding_grant_id>81771456 (to Cheng Zhou) and 81571353 (to Jin Liu)</funding_grant_id><pubmed_authors>Li H</pubmed_authors><pubmed_authors>Liu J</pubmed_authors><pubmed_authors>Zhou C</pubmed_authors><pubmed_authors>Zhao W</pubmed_authors><pubmed_authors>Liao D</pubmed_authors><pubmed_authors>Li Q</pubmed_authors><pubmed_authors>Chen X</pubmed_authors><pubmed_authors>Liang P</pubmed_authors></additional><is_claimable>false</is_claimable><name>Capsazepine prolongation of the duration of lidocaine block of sensory transmission in mice may be mediated by modulation of HCN channel currents.</name><description>&lt;h4>Background and objectives&lt;/h4>Hyperpolarization-activation cyclic nucleotide-gated (HCN) channels contribute to the effects of lidocaine. Capsazepine (CPZ), a competitive inhibitor of capsaicin of transient receptor potential vanilloid-1 channel, has also been found to inhibit HCN channel currents (&lt;i>I&lt;/i> &lt;sub>h&lt;/sub>). This study was designed to investigate whether CPZ could prolong durations of lidocaine in regional anesthesia.&lt;h4>Methods&lt;/h4>Mouse HCN1 and HCN2 channels were expressed in human embryonic kidney 293 (HEK 293) cells. The effect of CPZ on &lt;i>I&lt;/i> &lt;sub>h&lt;/sub> was measured by whole-cell patch-clamping recording. Sciatic nerve block model in mice was used for the study in vivo. The mice were randomly divided into seven groups, respectively, receiving lidocaine, CPZ, ZD</description><dates><release>2019-01-01T00:00:00Z</release><publication>2019</publication><modification>2025-04-04T22:09:17.012Z</modification><creation>2019-07-24T07:19:03Z</creation></dates><accession>S-EPMC6571133</accession><cross_references><pubmed>31223538</pubmed><doi>10.7717/peerj.7111</doi></cross_references></HashMap>