Adenosine monophosphate‐regulated protein kinase inhibition modulates electrophysiological characteristics and calcium homeostasis of rabbit right ventricular outflow tract
Background Metabolic stress predisposes to ventricular arrhythmias and sudden cardiac death. Right ventricular outflow tract (RVOT) is the common origin of ventricular arrhythmias. Adenosine monophosphate‐regulated protein kinase (AMPK) activation is an important compensatory mechanism for cardiac r...
Gespeichert in:
| Veröffentlicht in: | Fundamental & clinical pharmacology 2024-04, Vol.38 (2), p.262-275 |
|---|---|
| Hauptverfasser: | , , , , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | 275 |
|---|---|
| container_issue | 2 |
| container_start_page | 262 |
| container_title | Fundamental & clinical pharmacology |
| container_volume | 38 |
| creator | Lu, Yen‐Yu Cheng, Chen‐Chuan Chen, Yao‐Chang Lin, Yung‐Kuo Higa, Satoshi Kao, Yu‐Hsun Chen, Yi‐Jen |
| description | Background
Metabolic stress predisposes to ventricular arrhythmias and sudden cardiac death. Right ventricular outflow tract (RVOT) is the common origin of ventricular arrhythmias. Adenosine monophosphate‐regulated protein kinase (AMPK) activation is an important compensatory mechanism for cardiac remodeling during metabolic stress.
Objectives
The purpose of this study was to access whether AMPK inhibition would modulate RVOT electrophysiology, calcium (Ca2+) regulation, and RVOT arrhythmogenesis or not.
Methods
Conventional microelectrodes were used to record electrical activity before and after compound C (10 µM, an AMPK inhibitor) in isoproterenol (1 µM)‐treated rabbit RVOT tissue preparations under electrical pacing. Whole‐cell patch‐clamp and confocal microscopic examinations were performed in baseline and compound C‐treated rabbit RVOT cardiomyocytes to investigate ionic currents and intracellular Ca2+ transients in isolated rabbit RVOT cardiomyocytes.
Results
Compound C decreased RVOT contractility, and reversed isoproterenol increased RVOT contractility. Compound C decreased the incidence, rate, and duration of isoproterenol‐induced RVOT burst firing under rapid pacing. Compared to baseline, compound C‐treated RVOT cardiomyocytes had a longer action potential duration, smaller intracellular Ca2+ transients, late sodium (Na+), peak L‐type Ca2+ current density, Na+‐Ca2+ exchanger, transient outward potassium (K+) current, and rapid and slow delayed rectifier K+ currents.
Conclusion
AMPK inhibition modulates RVOT electrophysiological characteristics and Ca2+ homeostasis, contributing to lower RVOT arrhythmogenic activity. Accordingly, AMPK inhibition might potentially reduce ventricular tachyarrhythmias. |
| doi_str_mv | 10.1111/fcp.12953 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_2860619576</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>2955233757</sourcerecordid><originalsourceid>FETCH-LOGICAL-c3483-693cf058337d5ad30127b273f1e043acb678c1da388d04012e914f8aa36adfe33</originalsourceid><addsrcrecordid>eNp1kcFuFSEUhomxsdfqwhcwJG50MS0MM8AsmxurJk3aha4JA2fuUGdgBMbm7nwEn8SH8kmkvbULE9kccs7Hl0N-hF5RckrLORvMckrrrmVP0IY2oq5kTfhTtCGCi4p1kh6j5yndEEIFofwZOmaC80Z2coN-nVvwITkPeA4-LGNIy6gz_P7xM8JuncrV4iWGDM7jr87rBNj50fUuu-DLG3vPJAwTmByLYJ9cmMLOGT1hM-qoTYboUnYmYe0tLn3j1hmPYYaQsk4u4TDgqPvixNHtxoy_g8_RmaKOOKx5mMItznemF-ho0FOClw_1BH25eP95-7G6vPrwaXt-WRnWSFbxjpmBtJIxYVttGaG16GvBBgqkYdr0XEhDrWZSWtKUKXS0GaTWjGs7AGMn6O3BW77-bYWU1eySgWnSHsKaVC054bRrBS_om3_Qm7BGX7ZTJZK2Lju0olDvDpSJIaUIg1qim3XcK0rUXYiqhKjuQyzs6wfj2s9gH8m_qRXg7ADcugn2_zepi-31QfkHM4asuA</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2955233757</pqid></control><display><type>article</type><title>Adenosine monophosphate‐regulated protein kinase inhibition modulates electrophysiological characteristics and calcium homeostasis of rabbit right ventricular outflow tract</title><source>Wiley Online Library Journals Frontfile Complete</source><creator>Lu, Yen‐Yu ; Cheng, Chen‐Chuan ; Chen, Yao‐Chang ; Lin, Yung‐Kuo ; Higa, Satoshi ; Kao, Yu‐Hsun ; Chen, Yi‐Jen</creator><creatorcontrib>Lu, Yen‐Yu ; Cheng, Chen‐Chuan ; Chen, Yao‐Chang ; Lin, Yung‐Kuo ; Higa, Satoshi ; Kao, Yu‐Hsun ; Chen, Yi‐Jen</creatorcontrib><description>Background
Metabolic stress predisposes to ventricular arrhythmias and sudden cardiac death. Right ventricular outflow tract (RVOT) is the common origin of ventricular arrhythmias. Adenosine monophosphate‐regulated protein kinase (AMPK) activation is an important compensatory mechanism for cardiac remodeling during metabolic stress.
Objectives
The purpose of this study was to access whether AMPK inhibition would modulate RVOT electrophysiology, calcium (Ca2+) regulation, and RVOT arrhythmogenesis or not.
Methods
Conventional microelectrodes were used to record electrical activity before and after compound C (10 µM, an AMPK inhibitor) in isoproterenol (1 µM)‐treated rabbit RVOT tissue preparations under electrical pacing. Whole‐cell patch‐clamp and confocal microscopic examinations were performed in baseline and compound C‐treated rabbit RVOT cardiomyocytes to investigate ionic currents and intracellular Ca2+ transients in isolated rabbit RVOT cardiomyocytes.
Results
Compound C decreased RVOT contractility, and reversed isoproterenol increased RVOT contractility. Compound C decreased the incidence, rate, and duration of isoproterenol‐induced RVOT burst firing under rapid pacing. Compared to baseline, compound C‐treated RVOT cardiomyocytes had a longer action potential duration, smaller intracellular Ca2+ transients, late sodium (Na+), peak L‐type Ca2+ current density, Na+‐Ca2+ exchanger, transient outward potassium (K+) current, and rapid and slow delayed rectifier K+ currents.
Conclusion
AMPK inhibition modulates RVOT electrophysiological characteristics and Ca2+ homeostasis, contributing to lower RVOT arrhythmogenic activity. Accordingly, AMPK inhibition might potentially reduce ventricular tachyarrhythmias.</description><identifier>ISSN: 0767-3981</identifier><identifier>EISSN: 1472-8206</identifier><identifier>DOI: 10.1111/fcp.12953</identifier><identifier>PMID: 37664898</identifier><language>eng</language><publisher>England: Wiley Subscription Services, Inc</publisher><subject>Action potential ; Adenosine ; Adenosine kinase ; Adenosine monophosphate ; AMP ; AMP-activated protein kinase ; AMPK ; Calcium ; Calcium (intracellular) ; Calcium currents ; Calcium homeostasis ; Calcium ions ; Cardiac arrhythmia ; Cardiomyocytes ; Current density ; electrophysiological characteristics ; Electrophysiology ; Heart ; Homeostasis ; Intracellular ; Isoproterenol ; Kinases ; Metabolism ; Microelectrodes ; Muscle contraction ; Na+/Ca2+ exchanger ; Outflow ; Potassium ; Potassium currents ; Protein kinase ; Proteins ; Rabbits ; right ventricular outflow tract ; Sodium ; Ventricle ; ventricular arrhythmia</subject><ispartof>Fundamental & clinical pharmacology, 2024-04, Vol.38 (2), p.262-275</ispartof><rights>2023 Société Française de Pharmacologie et de Thérapeutique. Published by John Wiley & Sons Ltd</rights><rights>2023 Société Française de Pharmacologie et de Thérapeutique. Published by John Wiley & Sons Ltd.</rights><rights>2024 John Wiley & Sons, Ltd.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><cites>FETCH-LOGICAL-c3483-693cf058337d5ad30127b273f1e043acb678c1da388d04012e914f8aa36adfe33</cites><orcidid>0000-0002-6674-5625 ; 0000-0001-7224-4491 ; 0000-0002-3010-3209 ; 0000-0003-2624-8285 ; 0000-0002-5735-6249 ; 0000-0001-8687-5091 ; 0000-0001-6589-6993</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1111%2Ffcp.12953$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1111%2Ffcp.12953$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,776,780,1411,27901,27902,45550,45551</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/37664898$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Lu, Yen‐Yu</creatorcontrib><creatorcontrib>Cheng, Chen‐Chuan</creatorcontrib><creatorcontrib>Chen, Yao‐Chang</creatorcontrib><creatorcontrib>Lin, Yung‐Kuo</creatorcontrib><creatorcontrib>Higa, Satoshi</creatorcontrib><creatorcontrib>Kao, Yu‐Hsun</creatorcontrib><creatorcontrib>Chen, Yi‐Jen</creatorcontrib><title>Adenosine monophosphate‐regulated protein kinase inhibition modulates electrophysiological characteristics and calcium homeostasis of rabbit right ventricular outflow tract</title><title>Fundamental & clinical pharmacology</title><addtitle>Fundam Clin Pharmacol</addtitle><description>Background
Metabolic stress predisposes to ventricular arrhythmias and sudden cardiac death. Right ventricular outflow tract (RVOT) is the common origin of ventricular arrhythmias. Adenosine monophosphate‐regulated protein kinase (AMPK) activation is an important compensatory mechanism for cardiac remodeling during metabolic stress.
Objectives
The purpose of this study was to access whether AMPK inhibition would modulate RVOT electrophysiology, calcium (Ca2+) regulation, and RVOT arrhythmogenesis or not.
Methods
Conventional microelectrodes were used to record electrical activity before and after compound C (10 µM, an AMPK inhibitor) in isoproterenol (1 µM)‐treated rabbit RVOT tissue preparations under electrical pacing. Whole‐cell patch‐clamp and confocal microscopic examinations were performed in baseline and compound C‐treated rabbit RVOT cardiomyocytes to investigate ionic currents and intracellular Ca2+ transients in isolated rabbit RVOT cardiomyocytes.
Results
Compound C decreased RVOT contractility, and reversed isoproterenol increased RVOT contractility. Compound C decreased the incidence, rate, and duration of isoproterenol‐induced RVOT burst firing under rapid pacing. Compared to baseline, compound C‐treated RVOT cardiomyocytes had a longer action potential duration, smaller intracellular Ca2+ transients, late sodium (Na+), peak L‐type Ca2+ current density, Na+‐Ca2+ exchanger, transient outward potassium (K+) current, and rapid and slow delayed rectifier K+ currents.
Conclusion
AMPK inhibition modulates RVOT electrophysiological characteristics and Ca2+ homeostasis, contributing to lower RVOT arrhythmogenic activity. Accordingly, AMPK inhibition might potentially reduce ventricular tachyarrhythmias.</description><subject>Action potential</subject><subject>Adenosine</subject><subject>Adenosine kinase</subject><subject>Adenosine monophosphate</subject><subject>AMP</subject><subject>AMP-activated protein kinase</subject><subject>AMPK</subject><subject>Calcium</subject><subject>Calcium (intracellular)</subject><subject>Calcium currents</subject><subject>Calcium homeostasis</subject><subject>Calcium ions</subject><subject>Cardiac arrhythmia</subject><subject>Cardiomyocytes</subject><subject>Current density</subject><subject>electrophysiological characteristics</subject><subject>Electrophysiology</subject><subject>Heart</subject><subject>Homeostasis</subject><subject>Intracellular</subject><subject>Isoproterenol</subject><subject>Kinases</subject><subject>Metabolism</subject><subject>Microelectrodes</subject><subject>Muscle contraction</subject><subject>Na+/Ca2+ exchanger</subject><subject>Outflow</subject><subject>Potassium</subject><subject>Potassium currents</subject><subject>Protein kinase</subject><subject>Proteins</subject><subject>Rabbits</subject><subject>right ventricular outflow tract</subject><subject>Sodium</subject><subject>Ventricle</subject><subject>ventricular arrhythmia</subject><issn>0767-3981</issn><issn>1472-8206</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2024</creationdate><recordtype>article</recordtype><recordid>eNp1kcFuFSEUhomxsdfqwhcwJG50MS0MM8AsmxurJk3aha4JA2fuUGdgBMbm7nwEn8SH8kmkvbULE9kccs7Hl0N-hF5RckrLORvMckrrrmVP0IY2oq5kTfhTtCGCi4p1kh6j5yndEEIFofwZOmaC80Z2coN-nVvwITkPeA4-LGNIy6gz_P7xM8JuncrV4iWGDM7jr87rBNj50fUuu-DLG3vPJAwTmByLYJ9cmMLOGT1hM-qoTYboUnYmYe0tLn3j1hmPYYaQsk4u4TDgqPvixNHtxoy_g8_RmaKOOKx5mMItznemF-ho0FOClw_1BH25eP95-7G6vPrwaXt-WRnWSFbxjpmBtJIxYVttGaG16GvBBgqkYdr0XEhDrWZSWtKUKXS0GaTWjGs7AGMn6O3BW77-bYWU1eySgWnSHsKaVC054bRrBS_om3_Qm7BGX7ZTJZK2Lju0olDvDpSJIaUIg1qim3XcK0rUXYiqhKjuQyzs6wfj2s9gH8m_qRXg7ADcugn2_zepi-31QfkHM4asuA</recordid><startdate>202404</startdate><enddate>202404</enddate><creator>Lu, Yen‐Yu</creator><creator>Cheng, Chen‐Chuan</creator><creator>Chen, Yao‐Chang</creator><creator>Lin, Yung‐Kuo</creator><creator>Higa, Satoshi</creator><creator>Kao, Yu‐Hsun</creator><creator>Chen, Yi‐Jen</creator><general>Wiley Subscription Services, Inc</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7QL</scope><scope>7QO</scope><scope>7T7</scope><scope>7U7</scope><scope>7U9</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>H94</scope><scope>P64</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0002-6674-5625</orcidid><orcidid>https://orcid.org/0000-0001-7224-4491</orcidid><orcidid>https://orcid.org/0000-0002-3010-3209</orcidid><orcidid>https://orcid.org/0000-0003-2624-8285</orcidid><orcidid>https://orcid.org/0000-0002-5735-6249</orcidid><orcidid>https://orcid.org/0000-0001-8687-5091</orcidid><orcidid>https://orcid.org/0000-0001-6589-6993</orcidid></search><sort><creationdate>202404</creationdate><title>Adenosine monophosphate‐regulated protein kinase inhibition modulates electrophysiological characteristics and calcium homeostasis of rabbit right ventricular outflow tract</title><author>Lu, Yen‐Yu ; Cheng, Chen‐Chuan ; Chen, Yao‐Chang ; Lin, Yung‐Kuo ; Higa, Satoshi ; Kao, Yu‐Hsun ; Chen, Yi‐Jen</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3483-693cf058337d5ad30127b273f1e043acb678c1da388d04012e914f8aa36adfe33</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2024</creationdate><topic>Action potential</topic><topic>Adenosine</topic><topic>Adenosine kinase</topic><topic>Adenosine monophosphate</topic><topic>AMP</topic><topic>AMP-activated protein kinase</topic><topic>AMPK</topic><topic>Calcium</topic><topic>Calcium (intracellular)</topic><topic>Calcium currents</topic><topic>Calcium homeostasis</topic><topic>Calcium ions</topic><topic>Cardiac arrhythmia</topic><topic>Cardiomyocytes</topic><topic>Current density</topic><topic>electrophysiological characteristics</topic><topic>Electrophysiology</topic><topic>Heart</topic><topic>Homeostasis</topic><topic>Intracellular</topic><topic>Isoproterenol</topic><topic>Kinases</topic><topic>Metabolism</topic><topic>Microelectrodes</topic><topic>Muscle contraction</topic><topic>Na+/Ca2+ exchanger</topic><topic>Outflow</topic><topic>Potassium</topic><topic>Potassium currents</topic><topic>Protein kinase</topic><topic>Proteins</topic><topic>Rabbits</topic><topic>right ventricular outflow tract</topic><topic>Sodium</topic><topic>Ventricle</topic><topic>ventricular arrhythmia</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Lu, Yen‐Yu</creatorcontrib><creatorcontrib>Cheng, Chen‐Chuan</creatorcontrib><creatorcontrib>Chen, Yao‐Chang</creatorcontrib><creatorcontrib>Lin, Yung‐Kuo</creatorcontrib><creatorcontrib>Higa, Satoshi</creatorcontrib><creatorcontrib>Kao, Yu‐Hsun</creatorcontrib><creatorcontrib>Chen, Yi‐Jen</creatorcontrib><collection>PubMed</collection><collection>CrossRef</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Biotechnology Research Abstracts</collection><collection>Industrial and Applied Microbiology Abstracts (Microbiology A)</collection><collection>Toxicology Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Engineering Research Database</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Fundamental & clinical pharmacology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Lu, Yen‐Yu</au><au>Cheng, Chen‐Chuan</au><au>Chen, Yao‐Chang</au><au>Lin, Yung‐Kuo</au><au>Higa, Satoshi</au><au>Kao, Yu‐Hsun</au><au>Chen, Yi‐Jen</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Adenosine monophosphate‐regulated protein kinase inhibition modulates electrophysiological characteristics and calcium homeostasis of rabbit right ventricular outflow tract</atitle><jtitle>Fundamental & clinical pharmacology</jtitle><addtitle>Fundam Clin Pharmacol</addtitle><date>2024-04</date><risdate>2024</risdate><volume>38</volume><issue>2</issue><spage>262</spage><epage>275</epage><pages>262-275</pages><issn>0767-3981</issn><eissn>1472-8206</eissn><abstract>Background
Metabolic stress predisposes to ventricular arrhythmias and sudden cardiac death. Right ventricular outflow tract (RVOT) is the common origin of ventricular arrhythmias. Adenosine monophosphate‐regulated protein kinase (AMPK) activation is an important compensatory mechanism for cardiac remodeling during metabolic stress.
Objectives
The purpose of this study was to access whether AMPK inhibition would modulate RVOT electrophysiology, calcium (Ca2+) regulation, and RVOT arrhythmogenesis or not.
Methods
Conventional microelectrodes were used to record electrical activity before and after compound C (10 µM, an AMPK inhibitor) in isoproterenol (1 µM)‐treated rabbit RVOT tissue preparations under electrical pacing. Whole‐cell patch‐clamp and confocal microscopic examinations were performed in baseline and compound C‐treated rabbit RVOT cardiomyocytes to investigate ionic currents and intracellular Ca2+ transients in isolated rabbit RVOT cardiomyocytes.
Results
Compound C decreased RVOT contractility, and reversed isoproterenol increased RVOT contractility. Compound C decreased the incidence, rate, and duration of isoproterenol‐induced RVOT burst firing under rapid pacing. Compared to baseline, compound C‐treated RVOT cardiomyocytes had a longer action potential duration, smaller intracellular Ca2+ transients, late sodium (Na+), peak L‐type Ca2+ current density, Na+‐Ca2+ exchanger, transient outward potassium (K+) current, and rapid and slow delayed rectifier K+ currents.
Conclusion
AMPK inhibition modulates RVOT electrophysiological characteristics and Ca2+ homeostasis, contributing to lower RVOT arrhythmogenic activity. Accordingly, AMPK inhibition might potentially reduce ventricular tachyarrhythmias.</abstract><cop>England</cop><pub>Wiley Subscription Services, Inc</pub><pmid>37664898</pmid><doi>10.1111/fcp.12953</doi><tpages>14</tpages><orcidid>https://orcid.org/0000-0002-6674-5625</orcidid><orcidid>https://orcid.org/0000-0001-7224-4491</orcidid><orcidid>https://orcid.org/0000-0002-3010-3209</orcidid><orcidid>https://orcid.org/0000-0003-2624-8285</orcidid><orcidid>https://orcid.org/0000-0002-5735-6249</orcidid><orcidid>https://orcid.org/0000-0001-8687-5091</orcidid><orcidid>https://orcid.org/0000-0001-6589-6993</orcidid><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0767-3981 |
| ispartof | Fundamental & clinical pharmacology, 2024-04, Vol.38 (2), p.262-275 |
| issn | 0767-3981 1472-8206 |
| language | eng |
| recordid | cdi_proquest_miscellaneous_2860619576 |
| source | Wiley Online Library Journals Frontfile Complete |
| subjects | Action potential Adenosine Adenosine kinase Adenosine monophosphate AMP AMP-activated protein kinase AMPK Calcium Calcium (intracellular) Calcium currents Calcium homeostasis Calcium ions Cardiac arrhythmia Cardiomyocytes Current density electrophysiological characteristics Electrophysiology Heart Homeostasis Intracellular Isoproterenol Kinases Metabolism Microelectrodes Muscle contraction Na+/Ca2+ exchanger Outflow Potassium Potassium currents Protein kinase Proteins Rabbits right ventricular outflow tract Sodium Ventricle ventricular arrhythmia |
| title | Adenosine monophosphate‐regulated protein kinase inhibition modulates electrophysiological characteristics and calcium homeostasis of rabbit right ventricular outflow tract |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-02-06T14%3A26%3A38IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_cross&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Adenosine%20monophosphate%E2%80%90regulated%20protein%20kinase%20inhibition%20modulates%20electrophysiological%20characteristics%20and%20calcium%20homeostasis%20of%20rabbit%20right%20ventricular%20outflow%20tract&rft.jtitle=Fundamental%20&%20clinical%20pharmacology&rft.au=Lu,%20Yen%E2%80%90Yu&rft.date=2024-04&rft.volume=38&rft.issue=2&rft.spage=262&rft.epage=275&rft.pages=262-275&rft.issn=0767-3981&rft.eissn=1472-8206&rft_id=info:doi/10.1111/fcp.12953&rft_dat=%3Cproquest_cross%3E2955233757%3C/proquest_cross%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=2955233757&rft_id=info:pmid/37664898&rfr_iscdi=true |