<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Shi J</submitter><funding>British Heart Foundation</funding><pagination>2161-75</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC3402779</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>166(7)</volume><pubmed_abstract>&lt;h4>Background and purpose&lt;/h4>Endothelin(A) (ET(A) ) receptor-operated canonical transient receptor potential (TRPC) channels mediate Ca²⁺ influx pathways, which are important in coronary artery function. Biochemical pathways linking ET(A) receptor stimulation to TRPC channel opening are unknown. We investigated the involvement of phosphatidylinositol 3-kinases (PI3K) in ET(A) receptor activation of native heteromeric TRPC1/C5/C6 and TRPC3/C7 channels in rabbit coronary artery vascular smooth muscle cells (VSMCs).&lt;h4>Experimental approach&lt;/h4>A pharmacological profile of PI3K was created by studying the effect of pan-PI3K, pan-Class I PI3K and Class I PI3K isoform-selective inhibitors on ET(A) receptor-evoked single TRPC1/C5/C6 and TRPC3/C7 channel activities in cell-attached patches from</pubmed_abstract><journal>British journal of pharmacology</journal><pubmed_title>Pharmacological profile of phosphatidylinositol 3-kinases and related phosphatidylinositols mediating endothelin(A)  receptor-operated native TRPC channels in rabbit coronary artery myocytes.</pubmed_title><pmcid>PMC3402779</pmcid><funding_grant_id>PG/08/042/25066</funding_grant_id><funding_grant_id>PG/07/079/23568</funding_grant_id><pubmed_authors>Large WA</pubmed_authors><pubmed_authors>Albert AP</pubmed_authors><pubmed_authors>Ju M</pubmed_authors><pubmed_authors>Shi J</pubmed_authors></additional><is_claimable>false</is_claimable><name>Pharmacological profile of phosphatidylinositol 3-kinases and related phosphatidylinositols mediating endothelin(A)  receptor-operated native TRPC channels in rabbit coronary artery myocytes.</name><description>&lt;h4>Background and purpose&lt;/h4>Endothelin(A) (ET(A) ) receptor-operated canonical transient receptor potential (TRPC) channels mediate Ca²⁺ influx pathways, which are important in coronary artery function. Biochemical pathways linking ET(A) receptor stimulation to TRPC channel opening are unknown. We investigated the involvement of phosphatidylinositol 3-kinases (PI3K) in ET(A) receptor activation of native heteromeric TRPC1/C5/C6 and TRPC3/C7 channels in rabbit coronary artery vascular smooth muscle cells (VSMCs).&lt;h4>Experimental approach&lt;/h4>A pharmacological profile of PI3K was created by studying the effect of pan-PI3K, pan-Class I PI3K and Class I PI3K isoform-selective inhibitors on ET(A) receptor-evoked single TRPC1/C5/C6 and TRPC3/C7 channel activities in cell-attached patches from</description><dates><release>2012-01-01T00:00:00Z</release><publication>2012 Aug</publication><modification>2025-04-05T13:00:24.082Z</modification><creation>2019-03-27T00:55:52Z</creation></dates><accession>S-EPMC3402779</accession><cross_references><pubmed>22404177</pubmed><doi>10.1111/j.1476-5381.2012.01937.x</doi></cross_references></HashMap>