<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Narayanan D</submitter><funding>NHLBI NIH HHS</funding><pagination>631-41</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC3050675</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>107(5)</volume><pubmed_abstract>&lt;h4>Rationale&lt;/h4>Physiological functions of mitochondria in contractile arterial myocytes are poorly understood. Mitochondria can uptake calcium (Ca(2+)), but intracellular Ca(2+) signals that regulate mitochondrial Ca(2+) concentration ([Ca(2+)](mito)) and physiological functions of changes in [Ca(2+)](mito) in arterial myocytes are unclear.&lt;h4>Objective&lt;/h4>To identify Ca(2+) signals that regulate [Ca(2+)](mito), examine the significance of changes in [Ca(2+)](mito), and test the hypothesis that [Ca(2+)](mito) controls functional ion channel transcription in myocytes of resistance-size cerebral arteries.&lt;h4>Methods and results&lt;/h4>Endothelin (ET)-1 activated Ca(2+) waves and elevated global Ca(2+) concentration ([Ca(2+)](i)) via inositol 1,4,5-trisphosphate receptor (IP(3)R) activation.</pubmed_abstract><journal>Circulation research</journal><pubmed_title>Mitochondria control functional CaV1.2 expression in smooth muscle cells of cerebral arteries.</pubmed_title><pmcid>PMC3050675</pmcid><funding_grant_id>R01 HL067061-08</funding_grant_id><funding_grant_id>R01 HL077678-04</funding_grant_id><funding_grant_id>R01 HL077678-03</funding_grant_id><funding_grant_id>R01 HL067061-09</funding_grant_id><funding_grant_id>HL77678</funding_grant_id><funding_grant_id>R01 HL094378-01A1</funding_grant_id><funding_grant_id>R01 HL067061-07</funding_grant_id><funding_grant_id>R01 HL077678</funding_grant_id><funding_grant_id>R01 HL067061</funding_grant_id><funding_grant_id>HL67061</funding_grant_id><funding_grant_id>R01 HL094378</funding_grant_id><funding_grant_id>R01 HL077678-02</funding_grant_id><funding_grant_id>HL094378</funding_grant_id><funding_grant_id>R01 HL094378-02</funding_grant_id><pubmed_authors>Narayanan D</pubmed_authors><pubmed_authors>Xi Q</pubmed_authors><pubmed_authors>Jaggar JH</pubmed_authors><pubmed_authors>Pfeffer LM</pubmed_authors></additional><is_claimable>false</is_claimable><name>Mitochondria control functional CaV1.2 expression in smooth muscle cells of cerebral arteries.</name><description>&lt;h4>Rationale&lt;/h4>Physiological functions of mitochondria in contractile arterial myocytes are poorly understood. Mitochondria can uptake calcium (Ca(2+)), but intracellular Ca(2+) signals that regulate mitochondrial Ca(2+) concentration ([Ca(2+)](mito)) and physiological functions of changes in [Ca(2+)](mito) in arterial myocytes are unclear.&lt;h4>Objective&lt;/h4>To identify Ca(2+) signals that regulate [Ca(2+)](mito), examine the significance of changes in [Ca(2+)](mito), and test the hypothesis that [Ca(2+)](mito) controls functional ion channel transcription in myocytes of resistance-size cerebral arteries.&lt;h4>Methods and results&lt;/h4>Endothelin (ET)-1 activated Ca(2+) waves and elevated global Ca(2+) concentration ([Ca(2+)](i)) via inositol 1,4,5-trisphosphate receptor (IP(3)R) activation.</description><dates><release>2010-01-01T00:00:00Z</release><publication>2010 Sep</publication><modification>2025-04-20T03:59:33.997Z</modification><creation>2019-03-26T23:49:21Z</creation></dates><accession>S-EPMC3050675</accession><cross_references><pubmed>20616314</pubmed><doi>10.1161/circresaha.110.224345</doi><doi>10.1161/CIRCRESAHA.110.224345</doi></cross_references></HashMap>