30 Effects of angiotensin II on cytosolic calcium releases in isolated ventricular myocytes from adult normal and hypertensive rats

30 Effects of angiotensin II on cytosolic calcium releases in isolated ventricular myocytes from adult normal and hypertensive rats

METHODS:This study investigated the effects of angiotensin II (Ang II; 10-10mol/l) on calcium releases in ventricular myocytes from normal and renal hypertensive adult rats (Goldblatt two kidney one clip). Newly isolated myocytes were loaded with fluorescent indo-1/AM and studied at rest or under el...

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Veröffentlicht in:Journal of hypertension 1994-09, Vol.12 (9), p.1124-1124
Hauptverfasser: Sempe, S, Stuyvers, B, Tariosse, L, Gouverneur, G, Besse, P, Bonoron-Adèle, S
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container_end_page 1124
container_issue 9
container_start_page 1124
container_title Journal of hypertension
container_volume 12
creator Sempe, S
Stuyvers, B
Tariosse, L
Gouverneur, G
Besse, P
Bonoron-Adèle, S
description METHODS:This study investigated the effects of angiotensin II (Ang II; 10-10mol/l) on calcium releases in ventricular myocytes from normal and renal hypertensive adult rats (Goldblatt two kidney one clip). Newly isolated myocytes were loaded with fluorescent indo-1/AM and studied at rest or under electrical stimulation. The variation of the ratio of indo-1 emission (405/480 nm) was taken as a measure of cytosolic calcium variation. Five parameters were investigated from each peak systolic indo-1 ratio before and after Ang II additionamplitude variation, duration with analysis of a rise time and a fall time, and frequency of spontaneous calcium releases. RESULTS:The following changes were observed(1) in unstimulated myocytes exhibiting spontaneous contractile activity, an increase in the frequency of calcium transients, at 10mol/l, in normal cells (+157±27%, P
doi_str_mv 10.1097/00004872-199409000-00047
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Newly isolated myocytes were loaded with fluorescent indo-1/AM and studied at rest or under electrical stimulation. The variation of the ratio of indo-1 emission (405/480 nm) was taken as a measure of cytosolic calcium variation. Five parameters were investigated from each peak systolic indo-1 ratio before and after Ang II additionamplitude variation, duration with analysis of a rise time and a fall time, and frequency of spontaneous calcium releases. RESULTS:The following changes were observed(1) in unstimulated myocytes exhibiting spontaneous contractile activity, an increase in the frequency of calcium transients, at 10mol/l, in normal cells (+157±27%, P<0.01) and at each Ang II concentration in hypertrophied cells (+79±31%, P<0.01; +82±25%, P<0.01; +285±50%, P<0.01 at 10, 10 and 10 mol/l); (2) in stimulated myocytes, prolongation of the duration of calcium transients, explained by the occurrence of calcium releases during fall time. In addition, 50% of myocytes exhibited spontaneous releases of calcium in the interstimulus interval. The increase in calcium transient duration was statistically significant, regardless of the Ang II concentration in hypeitrophied cells (+36±20%, P<0.05; +39±18%, P 0.01; +77±34%, P<0.01 at 10, 10, 10mol/l) and only at 10mol/l in normal cells (+68±22%, P<0.01). Similar results were observed in fall time. CONCLUSION:Thus, in both normal and hypertrophied myocytes, Ang II induced calcium release, and hypertrophied cells became increasingly sensitive to Ang II. This occurrence of calcium release is a possible cause of arrhythmias, known as ‘triggered activity'.]]></description><identifier>ISSN: 0263-6352</identifier><identifier>EISSN: 1473-5598</identifier><identifier>DOI: 10.1097/00004872-199409000-00047</identifier><language>eng</language><publisher>Lippincott-Raven Publishers</publisher><ispartof>Journal of hypertension, 1994-09, Vol.12 (9), p.1124-1124</ispartof><rights>Lippincott-Raven Publishers.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27901,27902</link.rule.ids></links><search><creatorcontrib>Sempe, S</creatorcontrib><creatorcontrib>Stuyvers, B</creatorcontrib><creatorcontrib>Tariosse, L</creatorcontrib><creatorcontrib>Gouverneur, G</creatorcontrib><creatorcontrib>Besse, P</creatorcontrib><creatorcontrib>Bonoron-Adèle, S</creatorcontrib><title>30 Effects of angiotensin II on cytosolic calcium releases in isolated ventricular myocytes from adult normal and hypertensive rats</title><title>Journal of hypertension</title><description><![CDATA[METHODS:This study investigated the effects of angiotensin II (Ang II; 10-10mol/l) on calcium releases in ventricular myocytes from normal and renal hypertensive adult rats (Goldblatt two kidney one clip). Newly isolated myocytes were loaded with fluorescent indo-1/AM and studied at rest or under electrical stimulation. The variation of the ratio of indo-1 emission (405/480 nm) was taken as a measure of cytosolic calcium variation. Five parameters were investigated from each peak systolic indo-1 ratio before and after Ang II additionamplitude variation, duration with analysis of a rise time and a fall time, and frequency of spontaneous calcium releases. RESULTS:The following changes were observed(1) in unstimulated myocytes exhibiting spontaneous contractile activity, an increase in the frequency of calcium transients, at 10mol/l, in normal cells (+157±27%, P<0.01) and at each Ang II concentration in hypertrophied cells (+79±31%, P<0.01; +82±25%, P<0.01; +285±50%, P<0.01 at 10, 10 and 10 mol/l); (2) in stimulated myocytes, prolongation of the duration of calcium transients, explained by the occurrence of calcium releases during fall time. In addition, 50% of myocytes exhibited spontaneous releases of calcium in the interstimulus interval. The increase in calcium transient duration was statistically significant, regardless of the Ang II concentration in hypeitrophied cells (+36±20%, P<0.05; +39±18%, P 0.01; +77±34%, P<0.01 at 10, 10, 10mol/l) and only at 10mol/l in normal cells (+68±22%, P<0.01). Similar results were observed in fall time. CONCLUSION:Thus, in both normal and hypertrophied myocytes, Ang II induced calcium release, and hypertrophied cells became increasingly sensitive to Ang II. This occurrence of calcium release is a possible cause of arrhythmias, known as ‘triggered activity'.]]></description><issn>0263-6352</issn><issn>1473-5598</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1994</creationdate><recordtype>article</recordtype><recordid>eNp1UcFOwzAMjRBIjME_5AcKSZM0zRFNAyYhcdk98tKUFdJmStJNPfPjZBtwwxfL9nvP8jNCmJJ7SpR8IDl4LcuCKsWJylVx7MgLNKNcskIIVV-iGSkrVlRMlNfoJsaPDKmVZDP0xQhetq01KWLfYhjeO5_sELsBr1bYD9hMyUfvOoMNONONPQ7WWYg24ozp8giSbfDeDil0ZnQQcD_5zMqANvgeQzO6hAcfenBZv8HbaWfDacfe4gAp3qKrFly0dz95jtZPy_XipXh9e14tHl8Lo7gsGsVZxQirNhuihKrqUhgKgjSUQr6lLjmVFTFEmlJAXbVESMsEB7MxJRBl2BzVZ1kTfIzBtnoXuh7CpCnRRy_1r5f6z0t98jJT-Zl68C7ZED_deLBBby24tNX_vYB9A26veIk</recordid><startdate>199409</startdate><enddate>199409</enddate><creator>Sempe, S</creator><creator>Stuyvers, B</creator><creator>Tariosse, L</creator><creator>Gouverneur, G</creator><creator>Besse, P</creator><creator>Bonoron-Adèle, S</creator><general>Lippincott-Raven Publishers</general><scope>AAYXX</scope><scope>CITATION</scope></search><sort><creationdate>199409</creationdate><title>30 Effects of angiotensin II on cytosolic calcium releases in isolated ventricular myocytes from adult normal and hypertensive rats</title><author>Sempe, S ; Stuyvers, B ; Tariosse, L ; Gouverneur, G ; Besse, P ; Bonoron-Adèle, S</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c947-d94363036bb09596825c1a50d11a8978241760c07c25a86f057e354acbc2a09c3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1994</creationdate><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Sempe, S</creatorcontrib><creatorcontrib>Stuyvers, B</creatorcontrib><creatorcontrib>Tariosse, L</creatorcontrib><creatorcontrib>Gouverneur, G</creatorcontrib><creatorcontrib>Besse, P</creatorcontrib><creatorcontrib>Bonoron-Adèle, S</creatorcontrib><collection>CrossRef</collection><jtitle>Journal of hypertension</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Sempe, S</au><au>Stuyvers, B</au><au>Tariosse, L</au><au>Gouverneur, G</au><au>Besse, P</au><au>Bonoron-Adèle, S</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>30 Effects of angiotensin II on cytosolic calcium releases in isolated ventricular myocytes from adult normal and hypertensive rats</atitle><jtitle>Journal of hypertension</jtitle><date>1994-09</date><risdate>1994</risdate><volume>12</volume><issue>9</issue><spage>1124</spage><epage>1124</epage><pages>1124-1124</pages><issn>0263-6352</issn><eissn>1473-5598</eissn><abstract><![CDATA[METHODS:This study investigated the effects of angiotensin II (Ang II; 10-10mol/l) on calcium releases in ventricular myocytes from normal and renal hypertensive adult rats (Goldblatt two kidney one clip). Newly isolated myocytes were loaded with fluorescent indo-1/AM and studied at rest or under electrical stimulation. The variation of the ratio of indo-1 emission (405/480 nm) was taken as a measure of cytosolic calcium variation. Five parameters were investigated from each peak systolic indo-1 ratio before and after Ang II additionamplitude variation, duration with analysis of a rise time and a fall time, and frequency of spontaneous calcium releases. RESULTS:The following changes were observed(1) in unstimulated myocytes exhibiting spontaneous contractile activity, an increase in the frequency of calcium transients, at 10mol/l, in normal cells (+157±27%, P<0.01) and at each Ang II concentration in hypertrophied cells (+79±31%, P<0.01; +82±25%, P<0.01; +285±50%, P<0.01 at 10, 10 and 10 mol/l); (2) in stimulated myocytes, prolongation of the duration of calcium transients, explained by the occurrence of calcium releases during fall time. In addition, 50% of myocytes exhibited spontaneous releases of calcium in the interstimulus interval. The increase in calcium transient duration was statistically significant, regardless of the Ang II concentration in hypeitrophied cells (+36±20%, P<0.05; +39±18%, P 0.01; +77±34%, P<0.01 at 10, 10, 10mol/l) and only at 10mol/l in normal cells (+68±22%, P<0.01). Similar results were observed in fall time. CONCLUSION:Thus, in both normal and hypertrophied myocytes, Ang II induced calcium release, and hypertrophied cells became increasingly sensitive to Ang II. This occurrence of calcium release is a possible cause of arrhythmias, known as ‘triggered activity'.]]></abstract><pub>Lippincott-Raven Publishers</pub><doi>10.1097/00004872-199409000-00047</doi><tpages>1</tpages></addata></record>
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title 30 Effects of angiotensin II on cytosolic calcium releases in isolated ventricular myocytes from adult normal and hypertensive rats
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