Effect of carvedilol on ryanodine receptor in heart failure
The release of intracellular stores of Ca(2+) occurs virtually in all types of cells by a means of amplifying external signals that modulate intracellular signaling events. In cardiac myocytes, type 2 ryanodine receptor (RyR(2)) is activated during excitation-contraction (E-C) coupling by Ca(2+)-ind...
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| Veröffentlicht in: | Zhonghua er ke za zhi 2005-08, Vol.43 (8), p.603-607 |
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| creator | Li, Rong Yi, Qi-jian Qian, Yong-ru Liu, Xiao-yan |
| description | The release of intracellular stores of Ca(2+) occurs virtually in all types of cells by a means of amplifying external signals that modulate intracellular signaling events. In cardiac myocytes, type 2 ryanodine receptor (RyR(2)) is activated during excitation-contraction (E-C) coupling by Ca(2+)-induced Ca(2+) release (CICR) triggered by Ca(2+) influx across the sarcolemma. The hyperadrenergic state of heart failure results in leaky RyR(2) channels attributable to PKA hyperphosphorylation and depletion of the stabilizing FK506 binding protein, FKBP12.6. Dysregulation of sarcoplasmic reticulum (SR) Ca(2+) release via RyR(2) could contribute to defects in Ca(2+) signaling in failing hearts. Researchers tested the hypothesis that improved cardiac muscle function attributable to beta-AR blockade is associated with restoration of normal RyR(2) channel function in patients with heart failure. The authors aimed to observe change of RyR in junior mouse with HF and the effect of beta-adrenoreceptor blocker on RyR in H |
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In cardiac myocytes, type 2 ryanodine receptor (RyR(2)) is activated during excitation-contraction (E-C) coupling by Ca(2+)-induced Ca(2+) release (CICR) triggered by Ca(2+) influx across the sarcolemma. The hyperadrenergic state of heart failure results in leaky RyR(2) channels attributable to PKA hyperphosphorylation and depletion of the stabilizing FK506 binding protein, FKBP12.6. Dysregulation of sarcoplasmic reticulum (SR) Ca(2+) release via RyR(2) could contribute to defects in Ca(2+) signaling in failing hearts. Researchers tested the hypothesis that improved cardiac muscle function attributable to beta-AR blockade is associated with restoration of normal RyR(2) channel function in patients with heart failure. 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In cardiac myocytes, type 2 ryanodine receptor (RyR(2)) is activated during excitation-contraction (E-C) coupling by Ca(2+)-induced Ca(2+) release (CICR) triggered by Ca(2+) influx across the sarcolemma. The hyperadrenergic state of heart failure results in leaky RyR(2) channels attributable to PKA hyperphosphorylation and depletion of the stabilizing FK506 binding protein, FKBP12.6. Dysregulation of sarcoplasmic reticulum (SR) Ca(2+) release via RyR(2) could contribute to defects in Ca(2+) signaling in failing hearts. Researchers tested the hypothesis that improved cardiac muscle function attributable to beta-AR blockade is associated with restoration of normal RyR(2) channel function in patients with heart failure. The authors aimed to observe change of RyR in junior mouse with HF and the effect of beta-adrenoreceptor blocker on RyR in H</description><subject>Adrenergic beta-Antagonists - pharmacology</subject><subject>Animals</subject><subject>Animals, Newborn</subject><subject>Calcium - metabolism</subject><subject>Calcium Signaling - drug effects</subject><subject>Calcium-Transporting ATPases - antagonists & inhibitors</subject><subject>Carbazoles - pharmacology</subject><subject>Disease Models, Animal</subject><subject>Heart Failure - diagnostic imaging</subject><subject>Heart Failure - drug therapy</subject><subject>Heart Failure - metabolism</subject><subject>Myocardial Contraction - drug effects</subject><subject>Myocytes, Cardiac - drug effects</subject><subject>Myocytes, Cardiac - metabolism</subject><subject>Propanolamines - pharmacology</subject><subject>Rats</subject><subject>Rats, Wistar</subject><subject>Ryanodine Receptor Calcium Release Channel - metabolism</subject><subject>Sarcoplasmic Reticulum - drug effects</subject><subject>Sarcoplasmic Reticulum - metabolism</subject><subject>Spectrometry, Fluorescence</subject><subject>Thapsigargin - pharmacology</subject><subject>Ultrasonography</subject><issn>0578-1310</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2005</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNo1j01LxDAUAHNQ3GXdvyC5eSokfWna4kmW9QMWvOi5vCQvGEibmrTC_nsF19NchoG5YlvRtF0lQYoN25cSjACtVC0U3LCN1LKXdQtb9nD0nuzCk-cW8ze5EFPkaeL5jFNyYSKeydK8pMzDxD8J88I9hrhmumXXHmOh_YU79vF0fD-8VKe359fD46maZd0sFUGnHUp0zrhOKw9G9LqV1DUkOlANeeUbQ0Zp59Aq6b2wvTHWGS0sKoIdu__rzjl9rVSWYQzFUow4UVrL0AL0rRbQ_5p3F3M1I7lhzmHEfB7-f-EHX41SPQ</recordid><startdate>200508</startdate><enddate>200508</enddate><creator>Li, Rong</creator><creator>Yi, Qi-jian</creator><creator>Qian, Yong-ru</creator><creator>Liu, Xiao-yan</creator><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>7X8</scope></search><sort><creationdate>200508</creationdate><title>Effect of carvedilol on ryanodine receptor in heart failure</title><author>Li, Rong ; Yi, Qi-jian ; Qian, Yong-ru ; Liu, Xiao-yan</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-p125t-e386da1addbd864f3b09671e85e08345ef4f5beb46ddac41ff0c9bbcdb60ca4e3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>chi</language><creationdate>2005</creationdate><topic>Adrenergic beta-Antagonists - pharmacology</topic><topic>Animals</topic><topic>Animals, Newborn</topic><topic>Calcium - metabolism</topic><topic>Calcium Signaling - drug effects</topic><topic>Calcium-Transporting ATPases - antagonists & inhibitors</topic><topic>Carbazoles - pharmacology</topic><topic>Disease Models, Animal</topic><topic>Heart Failure - diagnostic imaging</topic><topic>Heart Failure - drug therapy</topic><topic>Heart Failure - metabolism</topic><topic>Myocardial Contraction - drug effects</topic><topic>Myocytes, Cardiac - drug effects</topic><topic>Myocytes, Cardiac - metabolism</topic><topic>Propanolamines - pharmacology</topic><topic>Rats</topic><topic>Rats, Wistar</topic><topic>Ryanodine Receptor Calcium Release Channel - metabolism</topic><topic>Sarcoplasmic Reticulum - drug effects</topic><topic>Sarcoplasmic Reticulum - metabolism</topic><topic>Spectrometry, Fluorescence</topic><topic>Thapsigargin - pharmacology</topic><topic>Ultrasonography</topic><toplevel>online_resources</toplevel><creatorcontrib>Li, Rong</creatorcontrib><creatorcontrib>Yi, Qi-jian</creatorcontrib><creatorcontrib>Qian, Yong-ru</creatorcontrib><creatorcontrib>Liu, Xiao-yan</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>MEDLINE - Academic</collection><jtitle>Zhonghua er ke za zhi</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Li, Rong</au><au>Yi, Qi-jian</au><au>Qian, Yong-ru</au><au>Liu, Xiao-yan</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Effect of carvedilol on ryanodine receptor in heart failure</atitle><jtitle>Zhonghua er ke za zhi</jtitle><addtitle>Zhonghua Er Ke Za Zhi</addtitle><date>2005-08</date><risdate>2005</risdate><volume>43</volume><issue>8</issue><spage>603</spage><epage>607</epage><pages>603-607</pages><issn>0578-1310</issn><abstract>The release of intracellular stores of Ca(2+) occurs virtually in all types of cells by a means of amplifying external signals that modulate intracellular signaling events. In cardiac myocytes, type 2 ryanodine receptor (RyR(2)) is activated during excitation-contraction (E-C) coupling by Ca(2+)-induced Ca(2+) release (CICR) triggered by Ca(2+) influx across the sarcolemma. The hyperadrenergic state of heart failure results in leaky RyR(2) channels attributable to PKA hyperphosphorylation and depletion of the stabilizing FK506 binding protein, FKBP12.6. Dysregulation of sarcoplasmic reticulum (SR) Ca(2+) release via RyR(2) could contribute to defects in Ca(2+) signaling in failing hearts. Researchers tested the hypothesis that improved cardiac muscle function attributable to beta-AR blockade is associated with restoration of normal RyR(2) channel function in patients with heart failure. The authors aimed to observe change of RyR in junior mouse with HF and the effect of beta-adrenoreceptor blocker on RyR in H</abstract><cop>China</cop><pmid>16191273</pmid><tpages>5</tpages></addata></record> |
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| source | MEDLINE; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals |
| subjects | Adrenergic beta-Antagonists - pharmacology Animals Animals, Newborn Calcium - metabolism Calcium Signaling - drug effects Calcium-Transporting ATPases - antagonists & inhibitors Carbazoles - pharmacology Disease Models, Animal Heart Failure - diagnostic imaging Heart Failure - drug therapy Heart Failure - metabolism Myocardial Contraction - drug effects Myocytes, Cardiac - drug effects Myocytes, Cardiac - metabolism Propanolamines - pharmacology Rats Rats, Wistar Ryanodine Receptor Calcium Release Channel - metabolism Sarcoplasmic Reticulum - drug effects Sarcoplasmic Reticulum - metabolism Spectrometry, Fluorescence Thapsigargin - pharmacology Ultrasonography |
| title | Effect of carvedilol on ryanodine receptor in heart failure |
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