Intracrine action of angiotensin II in the intact ventricle of the failing heart: angiotensin II changes cardiac excitability from within
The influence of intracellular injection of angiotensin II (Ang II) on electrical properties of single right ventricular fibers from the failing heart of cardiomyopathic hamsters (TO2) was investigated in the intact ventricle of 8-month-old animals. Intracellular injection was performed using pressu...
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| Veröffentlicht in: | Molecular and cellular biochemistry 2011-12, Vol.358 (1-2), p.309-315 |
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| description | The influence of intracellular injection of angiotensin II (Ang II) on electrical properties of single right ventricular fibers from the failing heart of cardiomyopathic hamsters (TO2) was investigated in the intact ventricle of 8-month-old animals. Intracellular injection was performed using pressure pulses (40–70 psi) for short periods of time (20 ms) while recoding the action potential simultaneously from the same fiber. The results indicated that intracellular Ang II caused a hyperpolarization of 7.7 mV ± 4.3 mV (
n
= 39) (4 animals) (
P
|
| doi_str_mv | 10.1007/s11010-011-0981-4 |
| format | Article |
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n
= 39) (4 animals) (
P
< 0.05) followed by a small fall in membrane potential. The action potential duration was significantly increased at 50% and at 90% repolarization, and the refractoriness was significantly enhanced. The effect of intracellular Ang II on action potential duration was related to the inhibition of potassium conductance through PKC activation because Bis-1 (360 nM), a selective PKC inhibitor, abolished the effect of the peptide. Injections performed in different fibers of the same ventricle showed a variable effect of Ang II on action potential duration and generated spontaneous rhythmicity. The effect of intracellular Ang II on action potential duration and cardiac refractoriness remains for more than 1 h after interruption of the intracellular injection of the peptide.</description><identifier>ISSN: 0300-8177</identifier><identifier>EISSN: 1573-4919</identifier><identifier>DOI: 10.1007/s11010-011-0981-4</identifier><identifier>PMID: 21744071</identifier><language>eng</language><publisher>Boston: Springer US</publisher><subject>Action Potentials - drug effects ; Angiotensin ; Angiotensin II - administration & dosage ; Angiotensin II - pharmacology ; Animals ; Biochemistry ; Biomedical and Life Sciences ; Cardiology ; Cardiovascular disease ; Cell Separation ; Cellular biology ; Cricetinae ; Electrical properties ; Enzymes ; Fibers ; Hamsters ; Heart ; Heart Failure - physiopathology ; Heart Ventricles - physiopathology ; In Vitro Techniques ; Injection ; Intracellular Space - drug effects ; Intracellular Space - metabolism ; Life Sciences ; Losartan - pharmacology ; Male ; Medical Biochemistry ; Myocytes, Cardiac - drug effects ; Myocytes, Cardiac - physiology ; Oncology ; Peptides ; Signal Transduction - drug effects</subject><ispartof>Molecular and cellular biochemistry, 2011-12, Vol.358 (1-2), p.309-315</ispartof><rights>Springer Science+Business Media, LLC. 2011</rights><rights>COPYRIGHT 2011 Springer</rights><rights>Springer Science+Business Media, LLC. 2011 2011</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c601t-1c8c7e9e7d2b82f76c7d9c66bccdaa01f522adda862e68200d5c81fae5dbc1623</citedby><cites>FETCH-LOGICAL-c601t-1c8c7e9e7d2b82f76c7d9c66bccdaa01f522adda862e68200d5c81fae5dbc1623</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s11010-011-0981-4$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s11010-011-0981-4$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>230,314,780,784,885,27923,27924,41487,42556,51318</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/21744071$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>De Mello, Walmor C.</creatorcontrib><title>Intracrine action of angiotensin II in the intact ventricle of the failing heart: angiotensin II changes cardiac excitability from within</title><title>Molecular and cellular biochemistry</title><addtitle>Mol Cell Biochem</addtitle><addtitle>Mol Cell Biochem</addtitle><description>The influence of intracellular injection of angiotensin II (Ang II) on electrical properties of single right ventricular fibers from the failing heart of cardiomyopathic hamsters (TO2) was investigated in the intact ventricle of 8-month-old animals. Intracellular injection was performed using pressure pulses (40–70 psi) for short periods of time (20 ms) while recoding the action potential simultaneously from the same fiber. The results indicated that intracellular Ang II caused a hyperpolarization of 7.7 mV ± 4.3 mV (
n
= 39) (4 animals) (
P
< 0.05) followed by a small fall in membrane potential. The action potential duration was significantly increased at 50% and at 90% repolarization, and the refractoriness was significantly enhanced. The effect of intracellular Ang II on action potential duration was related to the inhibition of potassium conductance through PKC activation because Bis-1 (360 nM), a selective PKC inhibitor, abolished the effect of the peptide. Injections performed in different fibers of the same ventricle showed a variable effect of Ang II on action potential duration and generated spontaneous rhythmicity. The effect of intracellular Ang II on action potential duration and cardiac refractoriness remains for more than 1 h after interruption of the intracellular injection of the peptide.</description><subject>Action Potentials - drug effects</subject><subject>Angiotensin</subject><subject>Angiotensin II - administration & dosage</subject><subject>Angiotensin II - pharmacology</subject><subject>Animals</subject><subject>Biochemistry</subject><subject>Biomedical and Life Sciences</subject><subject>Cardiology</subject><subject>Cardiovascular disease</subject><subject>Cell Separation</subject><subject>Cellular biology</subject><subject>Cricetinae</subject><subject>Electrical properties</subject><subject>Enzymes</subject><subject>Fibers</subject><subject>Hamsters</subject><subject>Heart</subject><subject>Heart Failure - physiopathology</subject><subject>Heart Ventricles - physiopathology</subject><subject>In Vitro Techniques</subject><subject>Injection</subject><subject>Intracellular Space - drug effects</subject><subject>Intracellular Space - metabolism</subject><subject>Life Sciences</subject><subject>Losartan - pharmacology</subject><subject>Male</subject><subject>Medical Biochemistry</subject><subject>Myocytes, Cardiac - drug effects</subject><subject>Myocytes, Cardiac - physiology</subject><subject>Oncology</subject><subject>Peptides</subject><subject>Signal Transduction - drug effects</subject><issn>0300-8177</issn><issn>1573-4919</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2011</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNp1kl1rFTEQhoMo9nj0B3gjQS-82prZj2TXC6EUPw4UvNHrkE1mz6bsJjXJqfYn9F83y9ZqixJIYOZ5h8zMS8hLYMfAmHgXARiwggEUrGuhqB-RDTSiKuoOusdkwyrGihaEOCLPYjxnGc7sU3JUgqhrJmBDrncuBaWDdUiVTtY76geq3N76hC5aR3c7mu80Yn5SRuglZonVEy7kEh-Unazb0xFVSO8fivWYAxipVsFYpSn-0japPkvSFR2Cn-lPm0brnpMng5oivrh9t-T7p4_fTr8UZ18_705PzgrNGaQCdKsFdihM2bflILgWptOc91obpRgMTVkqY1TLS-RtyZhpdAuDwsb0GnhZbcmHte7FoZ_R6KUbNcmLYGcVrqRXVt7PODvKvb-UlRBdlae7JW9vCwT_44AxydlGjdOkHPpDlN0yZs4ryOTrB-S5PwSXu8sQE6IWTZ2hNyu0VxNK6wa_LGQpKU-qpqsBQPBMHf-DysfgbLV3ONgcvyeAVaCDjzHgcNchMLm4R67ukdkRcnGPXL7y6u_R3Cl-2yUD5QrEnMpbDX8a-n_VG5d10XE</recordid><startdate>20111201</startdate><enddate>20111201</enddate><creator>De Mello, Walmor C.</creator><general>Springer US</general><general>Springer</general><general>Springer Nature B.V</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7QL</scope><scope>7QP</scope><scope>7T5</scope><scope>7T7</scope><scope>7TK</scope><scope>7TM</scope><scope>7TO</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>88I</scope><scope>8AO</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AEUYN</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M2P</scope><scope>M7N</scope><scope>M7P</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>Q9U</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20111201</creationdate><title>Intracrine action of angiotensin II in the intact ventricle of the failing heart: angiotensin II changes cardiac excitability from within</title><author>De Mello, Walmor C.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c601t-1c8c7e9e7d2b82f76c7d9c66bccdaa01f522adda862e68200d5c81fae5dbc1623</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2011</creationdate><topic>Action Potentials - drug effects</topic><topic>Angiotensin</topic><topic>Angiotensin II - administration & dosage</topic><topic>Angiotensin II - pharmacology</topic><topic>Animals</topic><topic>Biochemistry</topic><topic>Biomedical and Life Sciences</topic><topic>Cardiology</topic><topic>Cardiovascular disease</topic><topic>Cell Separation</topic><topic>Cellular biology</topic><topic>Cricetinae</topic><topic>Electrical properties</topic><topic>Enzymes</topic><topic>Fibers</topic><topic>Hamsters</topic><topic>Heart</topic><topic>Heart Failure - physiopathology</topic><topic>Heart Ventricles - physiopathology</topic><topic>In Vitro Techniques</topic><topic>Injection</topic><topic>Intracellular Space - drug effects</topic><topic>Intracellular Space - metabolism</topic><topic>Life Sciences</topic><topic>Losartan - pharmacology</topic><topic>Male</topic><topic>Medical Biochemistry</topic><topic>Myocytes, Cardiac - drug effects</topic><topic>Myocytes, Cardiac - physiology</topic><topic>Oncology</topic><topic>Peptides</topic><topic>Signal Transduction - 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Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Molecular and cellular biochemistry</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>De Mello, Walmor C.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Intracrine action of angiotensin II in the intact ventricle of the failing heart: angiotensin II changes cardiac excitability from within</atitle><jtitle>Molecular and cellular biochemistry</jtitle><stitle>Mol Cell Biochem</stitle><addtitle>Mol Cell Biochem</addtitle><date>2011-12-01</date><risdate>2011</risdate><volume>358</volume><issue>1-2</issue><spage>309</spage><epage>315</epage><pages>309-315</pages><issn>0300-8177</issn><eissn>1573-4919</eissn><abstract>The influence of intracellular injection of angiotensin II (Ang II) on electrical properties of single right ventricular fibers from the failing heart of cardiomyopathic hamsters (TO2) was investigated in the intact ventricle of 8-month-old animals. Intracellular injection was performed using pressure pulses (40–70 psi) for short periods of time (20 ms) while recoding the action potential simultaneously from the same fiber. The results indicated that intracellular Ang II caused a hyperpolarization of 7.7 mV ± 4.3 mV (
n
= 39) (4 animals) (
P
< 0.05) followed by a small fall in membrane potential. The action potential duration was significantly increased at 50% and at 90% repolarization, and the refractoriness was significantly enhanced. The effect of intracellular Ang II on action potential duration was related to the inhibition of potassium conductance through PKC activation because Bis-1 (360 nM), a selective PKC inhibitor, abolished the effect of the peptide. Injections performed in different fibers of the same ventricle showed a variable effect of Ang II on action potential duration and generated spontaneous rhythmicity. The effect of intracellular Ang II on action potential duration and cardiac refractoriness remains for more than 1 h after interruption of the intracellular injection of the peptide.</abstract><cop>Boston</cop><pub>Springer US</pub><pmid>21744071</pmid><doi>10.1007/s11010-011-0981-4</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Molecular and cellular biochemistry, 2011-12, Vol.358 (1-2), p.309-315 |
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| subjects | Action Potentials - drug effects Angiotensin Angiotensin II - administration & dosage Angiotensin II - pharmacology Animals Biochemistry Biomedical and Life Sciences Cardiology Cardiovascular disease Cell Separation Cellular biology Cricetinae Electrical properties Enzymes Fibers Hamsters Heart Heart Failure - physiopathology Heart Ventricles - physiopathology In Vitro Techniques Injection Intracellular Space - drug effects Intracellular Space - metabolism Life Sciences Losartan - pharmacology Male Medical Biochemistry Myocytes, Cardiac - drug effects Myocytes, Cardiac - physiology Oncology Peptides Signal Transduction - drug effects |
| title | Intracrine action of angiotensin II in the intact ventricle of the failing heart: angiotensin II changes cardiac excitability from within |
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