Hypotonically induced calcium increase and regulatory volume decrease in newborn rat cardiomyocytes
The effect of cell swelling on intracellular calcium concentration ([Ca2+]i) was studied in newborn rat cardiomyocytes. Hypotonic cell swelling induced a fast and transient [Ca2+]i increase (hypotonically induced calcium increase, HICI; 388±47 nM, n=14). HICI was not inhibited by cyclopiazonic acid...
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| Veröffentlicht in: | Pflügers Archiv 1998-07, Vol.436 (4), p.565-574 |
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| description | The effect of cell swelling on intracellular calcium concentration ([Ca2+]i) was studied in newborn rat cardiomyocytes. Hypotonic cell swelling induced a fast and transient [Ca2+]i increase (hypotonically induced calcium increase, HICI; 388±47 nM, n=14). HICI was not inhibited by cyclopiazonic acid (CPA), an inhibitor of sarcoplasmic Ca2+-ATPase, nor ryanodine (an inhibitor of calcium-induced calcium release), whereas it was abolished (11±19 nM, n=5) in the absence of external calcium. Thus, HICI appeared to depend exclusively on entry of external calcium. Gadolinium ion (Gd3+), a generic inhibitor of stretch-activated cation channels (SACs), was unable to affect HICI (353±79 nM, n=6). Similarly, HICI was unaffected by internal Na+ depletion and external Na+ omission. These results suggest that neither Gd3+-sensitive SACs nor Na+-Ca2+ exchange is responsible for HICI. Conversely, HICI was inhibited by diltiazem (42±4 nM, n=3) and by membrane predepolarization (40±18 nM, n=5), suggesting an involvement of L-type voltage-activated calciumchannels. Cardiomyocyte swelling was followed by a regulatory volume decrease (RVD). The putative role of HICI in volume regulation was studied by removal of external calcium. This procedure significantly slowed RVD but did not abolish it. In conclusion, newborn rat cardiomyocytes exhibit an external-calcium-dependent HICI which contributes partially to the RVD. |
| doi_str_mv | 10.1007/s004240050673 |
| format | Article |
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Hypotonic cell swelling induced a fast and transient [Ca2+]i increase (hypotonically induced calcium increase, HICI; 388±47 nM, n=14). HICI was not inhibited by cyclopiazonic acid (CPA), an inhibitor of sarcoplasmic Ca2+-ATPase, nor ryanodine (an inhibitor of calcium-induced calcium release), whereas it was abolished (11±19 nM, n=5) in the absence of external calcium. Thus, HICI appeared to depend exclusively on entry of external calcium. Gadolinium ion (Gd3+), a generic inhibitor of stretch-activated cation channels (SACs), was unable to affect HICI (353±79 nM, n=6). Similarly, HICI was unaffected by internal Na+ depletion and external Na+ omission. These results suggest that neither Gd3+-sensitive SACs nor Na+-Ca2+ exchange is responsible for HICI. Conversely, HICI was inhibited by diltiazem (42±4 nM, n=3) and by membrane predepolarization (40±18 nM, n=5), suggesting an involvement of L-type voltage-activated calciumchannels. Cardiomyocyte swelling was followed by a regulatory volume decrease (RVD). The putative role of HICI in volume regulation was studied by removal of external calcium. This procedure significantly slowed RVD but did not abolish it. In conclusion, newborn rat cardiomyocytes exhibit an external-calcium-dependent HICI which contributes partially to the RVD.</description><identifier>ISSN: 0031-6768</identifier><identifier>EISSN: 1432-2013</identifier><identifier>DOI: 10.1007/s004240050673</identifier><identifier>PMID: 9683730</identifier><language>eng</language><publisher>Germany: Springer Nature B.V</publisher><subject>Animals ; Animals, Newborn ; Ca super(2+)-transporting ATPase ; Calcium ; Calcium - metabolism ; Calcium Channel Blockers - pharmacology ; Calcium Channels - metabolism ; Cardiomyocytes ; Cell Size ; Diltiazem - pharmacology ; Fluorescent Dyes - metabolism ; Fura-2 - metabolism ; Gadolinium - metabolism ; Hypotonic Solutions ; Membrane Potentials - physiology ; Myocytes, Cardiac - cytology ; Myocytes, Cardiac - drug effects ; Myocytes, Cardiac - metabolism ; Osmolar Concentration ; Rats ; Rodents ; Sodium - metabolism</subject><ispartof>Pflügers Archiv, 1998-07, Vol.436 (4), p.565-574</ispartof><rights>Springer-Verlag Berlin Heidelberg 1998</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c415t-2dce8e6a478805d67047203809d4303d5b529bd229d122737e5ed410eb6b0e243</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/9683730$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Taouil, K</creatorcontrib><creatorcontrib>Giancola, R</creatorcontrib><creatorcontrib>Morel, J E</creatorcontrib><creatorcontrib>Hannaert, P</creatorcontrib><title>Hypotonically induced calcium increase and regulatory volume decrease in newborn rat cardiomyocytes</title><title>Pflügers Archiv</title><addtitle>Pflugers Arch</addtitle><description>The effect of cell swelling on intracellular calcium concentration ([Ca2+]i) was studied in newborn rat cardiomyocytes. Hypotonic cell swelling induced a fast and transient [Ca2+]i increase (hypotonically induced calcium increase, HICI; 388±47 nM, n=14). HICI was not inhibited by cyclopiazonic acid (CPA), an inhibitor of sarcoplasmic Ca2+-ATPase, nor ryanodine (an inhibitor of calcium-induced calcium release), whereas it was abolished (11±19 nM, n=5) in the absence of external calcium. Thus, HICI appeared to depend exclusively on entry of external calcium. Gadolinium ion (Gd3+), a generic inhibitor of stretch-activated cation channels (SACs), was unable to affect HICI (353±79 nM, n=6). Similarly, HICI was unaffected by internal Na+ depletion and external Na+ omission. These results suggest that neither Gd3+-sensitive SACs nor Na+-Ca2+ exchange is responsible for HICI. Conversely, HICI was inhibited by diltiazem (42±4 nM, n=3) and by membrane predepolarization (40±18 nM, n=5), suggesting an involvement of L-type voltage-activated calciumchannels. Cardiomyocyte swelling was followed by a regulatory volume decrease (RVD). The putative role of HICI in volume regulation was studied by removal of external calcium. This procedure significantly slowed RVD but did not abolish it. In conclusion, newborn rat cardiomyocytes exhibit an external-calcium-dependent HICI which contributes partially to the RVD.</description><subject>Animals</subject><subject>Animals, Newborn</subject><subject>Ca super(2+)-transporting ATPase</subject><subject>Calcium</subject><subject>Calcium - metabolism</subject><subject>Calcium Channel Blockers - pharmacology</subject><subject>Calcium Channels - metabolism</subject><subject>Cardiomyocytes</subject><subject>Cell Size</subject><subject>Diltiazem - pharmacology</subject><subject>Fluorescent Dyes - metabolism</subject><subject>Fura-2 - metabolism</subject><subject>Gadolinium - metabolism</subject><subject>Hypotonic Solutions</subject><subject>Membrane Potentials - physiology</subject><subject>Myocytes, Cardiac - cytology</subject><subject>Myocytes, Cardiac - drug effects</subject><subject>Myocytes, Cardiac - metabolism</subject><subject>Osmolar Concentration</subject><subject>Rats</subject><subject>Rodents</subject><subject>Sodium - metabolism</subject><issn>0031-6768</issn><issn>1432-2013</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1998</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>eNp90U1LxDAQBuAgyrquHj0KxYteqpOPNslRFr9gwYueS5rMSpe2WZNW6b-3yxZBD57CkGdeGF5CzincUAB5GwEEEwAZ5JIfkDkVnKUMKD8kcwBO01zm6picxLgBACYUm5GZzhWXHObEPg1b3_m2sqauh6RqXW_RJeNkq74ZZxvQRExM65KA731tOh-G5NPXfYOJw-m7apMWv0of2iSYblwPrvLN4O3QYTwlR2tTRzyb3gV5e7h_XT6lq5fH5-XdKrWCZl3KnEWFuRFSKchcLkFIBlyBdoIDd1mZMV06xrSjjEkuMUMnKGCZl4BM8AW52udug__oMXZFU0WLdW1a9H0sVA5cayF38vpfSUFzkWlNYaSXf-jG96Ed7yiUFMC4YHpE6R7Z4GMMuC62oWpMGMakYtdS8aul0V9MoX3ZoPvRUy38G-jei_g</recordid><startdate>199807</startdate><enddate>199807</enddate><creator>Taouil, K</creator><creator>Giancola, R</creator><creator>Morel, J E</creator><creator>Hannaert, P</creator><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>7QP</scope><scope>7TK</scope><scope>7TS</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>8AO</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>7X8</scope></search><sort><creationdate>199807</creationdate><title>Hypotonically induced calcium increase and regulatory volume decrease in newborn rat cardiomyocytes</title><author>Taouil, K ; Giancola, R ; Morel, J E ; Hannaert, P</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c415t-2dce8e6a478805d67047203809d4303d5b529bd229d122737e5ed410eb6b0e243</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1998</creationdate><topic>Animals</topic><topic>Animals, Newborn</topic><topic>Ca super(2+)-transporting ATPase</topic><topic>Calcium</topic><topic>Calcium - metabolism</topic><topic>Calcium Channel Blockers - pharmacology</topic><topic>Calcium Channels - metabolism</topic><topic>Cardiomyocytes</topic><topic>Cell Size</topic><topic>Diltiazem - pharmacology</topic><topic>Fluorescent Dyes - metabolism</topic><topic>Fura-2 - metabolism</topic><topic>Gadolinium - metabolism</topic><topic>Hypotonic Solutions</topic><topic>Membrane Potentials - physiology</topic><topic>Myocytes, Cardiac - cytology</topic><topic>Myocytes, Cardiac - drug effects</topic><topic>Myocytes, Cardiac - metabolism</topic><topic>Osmolar Concentration</topic><topic>Rats</topic><topic>Rodents</topic><topic>Sodium - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Taouil, K</creatorcontrib><creatorcontrib>Giancola, R</creatorcontrib><creatorcontrib>Morel, J E</creatorcontrib><creatorcontrib>Hannaert, P</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Physical Education Index</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Biology Database (Alumni Edition)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Biological Science Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>MEDLINE - Academic</collection><jtitle>Pflügers Archiv</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Taouil, K</au><au>Giancola, R</au><au>Morel, J E</au><au>Hannaert, P</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Hypotonically induced calcium increase and regulatory volume decrease in newborn rat cardiomyocytes</atitle><jtitle>Pflügers Archiv</jtitle><addtitle>Pflugers Arch</addtitle><date>1998-07</date><risdate>1998</risdate><volume>436</volume><issue>4</issue><spage>565</spage><epage>574</epage><pages>565-574</pages><issn>0031-6768</issn><eissn>1432-2013</eissn><abstract>The effect of cell swelling on intracellular calcium concentration ([Ca2+]i) was studied in newborn rat cardiomyocytes. Hypotonic cell swelling induced a fast and transient [Ca2+]i increase (hypotonically induced calcium increase, HICI; 388±47 nM, n=14). HICI was not inhibited by cyclopiazonic acid (CPA), an inhibitor of sarcoplasmic Ca2+-ATPase, nor ryanodine (an inhibitor of calcium-induced calcium release), whereas it was abolished (11±19 nM, n=5) in the absence of external calcium. Thus, HICI appeared to depend exclusively on entry of external calcium. Gadolinium ion (Gd3+), a generic inhibitor of stretch-activated cation channels (SACs), was unable to affect HICI (353±79 nM, n=6). Similarly, HICI was unaffected by internal Na+ depletion and external Na+ omission. These results suggest that neither Gd3+-sensitive SACs nor Na+-Ca2+ exchange is responsible for HICI. Conversely, HICI was inhibited by diltiazem (42±4 nM, n=3) and by membrane predepolarization (40±18 nM, n=5), suggesting an involvement of L-type voltage-activated calciumchannels. Cardiomyocyte swelling was followed by a regulatory volume decrease (RVD). The putative role of HICI in volume regulation was studied by removal of external calcium. This procedure significantly slowed RVD but did not abolish it. In conclusion, newborn rat cardiomyocytes exhibit an external-calcium-dependent HICI which contributes partially to the RVD.</abstract><cop>Germany</cop><pub>Springer Nature B.V</pub><pmid>9683730</pmid><doi>10.1007/s004240050673</doi><tpages>10</tpages></addata></record> |
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| subjects | Animals Animals, Newborn Ca super(2+)-transporting ATPase Calcium Calcium - metabolism Calcium Channel Blockers - pharmacology Calcium Channels - metabolism Cardiomyocytes Cell Size Diltiazem - pharmacology Fluorescent Dyes - metabolism Fura-2 - metabolism Gadolinium - metabolism Hypotonic Solutions Membrane Potentials - physiology Myocytes, Cardiac - cytology Myocytes, Cardiac - drug effects Myocytes, Cardiac - metabolism Osmolar Concentration Rats Rodents Sodium - metabolism |
| title | Hypotonically induced calcium increase and regulatory volume decrease in newborn rat cardiomyocytes |
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