The arrhythmogenic transient inward current iTI and related contraction in isolated guinea-pig ventricular myocytes

1. The arrhythmogenic transient inward current, iTI, and contractions were recorded in isolated guinea-pig ventricular myocytes, after exposure to strophanthidin or low external K+ (0.5 mM), using a single-microelectrode voltage-clamp technique and an optical measure of contraction. 2. The inward cu...

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Veröffentlicht in:The Journal of physiology 1987-11, Vol.392 (1), p.523-542
Hauptverfasser: Fedida, D, Noble, D, Rankin, A C, Spindler, A J
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Rankin, A C
Spindler, A J
description 1. The arrhythmogenic transient inward current, iTI, and contractions were recorded in isolated guinea-pig ventricular myocytes, after exposure to strophanthidin or low external K+ (0.5 mM), using a single-microelectrode voltage-clamp technique and an optical measure of contraction. 2. The inward current, iTI, and after-contraction occurred on repolarization after a depolarizing pre-pulse. Longer pre-pulses to more positive potentials increased the size and reduced the latency of iTI. Oscillatory currents and contractions also occurred during pulses to positive potentials. 3. The voltage dependence of iTI was studied by repolarizing to different potentials after a constant depolarizing pulse. Inward currents preceded after-contractions at all potentials. The iTI was maximal at about -50 mV, diminishing in magnitude at more negative and positive potentials. It remained inward at potentials up to +47 mV. The contraction exhibited a similar voltage dependence. The current-voltage relation varied in the same cell with longer exposure to glycosides. Thus, the voltage dependence of iTI reflected not only that of an underlying ionic mechanism but also the effects of potential on intracellular Ca2+ oscillations which trigger iTI. 4. Uniformity of internal Ca2+ transients was achieved by clamping to different potentials at the peak of an inward current. The iTI remained inward at positive potentials. An inward tail current, seen on repolarizing during iTI at the end of a depolarizing pre-pulse, progressively increased at negative potentials. This voltage dependence may be close to that of the Ca2+-activated inward current responsible for iTI. 5. Replacement of Na+ by Li+ initially increased the magnitude of iTI, but further exposure abolished the inward current, while the after-contractions continued to increase. The potential dependence of iTI was not affected by exposure to zero Na+. Replacement of Ca2+ by Sr2+ also abolished iTI and the after-contraction, but the main effect was to slow their occurrence. 6. The voltage dependence of the Ca2+-activated inward current in guinea-pig ventricular myocytes leads us to favour electrogenic Na-Ca exchange current as a major component of iTI, under our experimental conditions.
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The arrhythmogenic transient inward current, iTI, and contractions were recorded in isolated guinea-pig ventricular myocytes, after exposure to strophanthidin or low external K+ (0.5 mM), using a single-microelectrode voltage-clamp technique and an optical measure of contraction. 2. The inward current, iTI, and after-contraction occurred on repolarization after a depolarizing pre-pulse. Longer pre-pulses to more positive potentials increased the size and reduced the latency of iTI. Oscillatory currents and contractions also occurred during pulses to positive potentials. 3. The voltage dependence of iTI was studied by repolarizing to different potentials after a constant depolarizing pulse. Inward currents preceded after-contractions at all potentials. The iTI was maximal at about -50 mV, diminishing in magnitude at more negative and positive potentials. It remained inward at potentials up to +47 mV. The contraction exhibited a similar voltage dependence. The current-voltage relation varied in the same cell with longer exposure to glycosides. Thus, the voltage dependence of iTI reflected not only that of an underlying ionic mechanism but also the effects of potential on intracellular Ca2+ oscillations which trigger iTI. 4. Uniformity of internal Ca2+ transients was achieved by clamping to different potentials at the peak of an inward current. The iTI remained inward at positive potentials. An inward tail current, seen on repolarizing during iTI at the end of a depolarizing pre-pulse, progressively increased at negative potentials. This voltage dependence may be close to that of the Ca2+-activated inward current responsible for iTI. 5. Replacement of Na+ by Li+ initially increased the magnitude of iTI, but further exposure abolished the inward current, while the after-contractions continued to increase. The potential dependence of iTI was not affected by exposure to zero Na+. Replacement of Ca2+ by Sr2+ also abolished iTI and the after-contraction, but the main effect was to slow their occurrence. 6. The voltage dependence of the Ca2+-activated inward current in guinea-pig ventricular myocytes leads us to favour electrogenic Na-Ca exchange current as a major component of iTI, under our experimental conditions.</description><identifier>ISSN: 0022-3751</identifier><identifier>EISSN: 1469-7793</identifier><identifier>DOI: 10.1113/jphysiol.1987.sp016795</identifier><identifier>PMID: 2451728</identifier><identifier>CODEN: JPHYA7</identifier><language>eng</language><publisher>Oxford: The Physiological Society</publisher><subject>Action Potentials - drug effects ; Animals ; Biological and medical sciences ; Calcium - physiology ; Cells, Cultured ; Fundamental and applied biological sciences. 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The arrhythmogenic transient inward current, iTI, and contractions were recorded in isolated guinea-pig ventricular myocytes, after exposure to strophanthidin or low external K+ (0.5 mM), using a single-microelectrode voltage-clamp technique and an optical measure of contraction. 2. The inward current, iTI, and after-contraction occurred on repolarization after a depolarizing pre-pulse. Longer pre-pulses to more positive potentials increased the size and reduced the latency of iTI. Oscillatory currents and contractions also occurred during pulses to positive potentials. 3. The voltage dependence of iTI was studied by repolarizing to different potentials after a constant depolarizing pulse. Inward currents preceded after-contractions at all potentials. The iTI was maximal at about -50 mV, diminishing in magnitude at more negative and positive potentials. It remained inward at potentials up to +47 mV. The contraction exhibited a similar voltage dependence. The current-voltage relation varied in the same cell with longer exposure to glycosides. Thus, the voltage dependence of iTI reflected not only that of an underlying ionic mechanism but also the effects of potential on intracellular Ca2+ oscillations which trigger iTI. 4. Uniformity of internal Ca2+ transients was achieved by clamping to different potentials at the peak of an inward current. The iTI remained inward at positive potentials. An inward tail current, seen on repolarizing during iTI at the end of a depolarizing pre-pulse, progressively increased at negative potentials. This voltage dependence may be close to that of the Ca2+-activated inward current responsible for iTI. 5. Replacement of Na+ by Li+ initially increased the magnitude of iTI, but further exposure abolished the inward current, while the after-contractions continued to increase. The potential dependence of iTI was not affected by exposure to zero Na+. Replacement of Ca2+ by Sr2+ also abolished iTI and the after-contraction, but the main effect was to slow their occurrence. 6. The voltage dependence of the Ca2+-activated inward current in guinea-pig ventricular myocytes leads us to favour electrogenic Na-Ca exchange current as a major component of iTI, under our experimental conditions.</description><subject>Action Potentials - drug effects</subject><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Calcium - physiology</subject><subject>Cells, Cultured</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Guinea Pigs</subject><subject>Heart</subject><subject>Heart - physiology</subject><subject>In Vitro Techniques</subject><subject>Ion Channels - physiology</subject><subject>Myocardial Contraction</subject><subject>Potassium - pharmacology</subject><subject>Sodium - pharmacology</subject><subject>Strontium - pharmacology</subject><subject>Strophanthidin - pharmacology</subject><subject>Time Factors</subject><subject>Ventricular Function</subject><subject>Vertebrates: cardiovascular system</subject><issn>0022-3751</issn><issn>1469-7793</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1987</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkc1u1DAUhS0EKtPCI4CyQHSVwddO4niDBBU_RZVgMawtx3ESV4kd7KSjvD0OmY5gx8ryvd8550oHodeA9wBA392P3RKM6_fAS7YPI4aC8fwJ2kFW8JQxTp-iHcaEpJTl8BxdhnCPMVDM-QW6IFkOjJQ7FA6dTqT33TJ1g2u1NSqZvLTBaDslxh6lrxM1e__ne7hNpK0Tr3s56Th3NrJqMs5GNDHBbfN2NlbLdDRt8hB13qi5lz4ZFqeWSYcX6Fkj-6Bfnt4r9PPzp8PN1_Tu-5fbmw93qcp5TtO6pkWdAydVUelG16wiWVFloCjgpuGsJsDzipKC5ooVJOOUaELrgpclwaCBXqH3m-84V4Ou1XqK7MXozSD9Ipw04t-NNZ1o3YOAGEqBR4O3JwPvfs06TGIwQem-l1a7OQhWYpwVlESw2EDlXQheN-cQwGKtSzzWJda6xGNdUfjq7xPPslM_cf_mtJdByb6JzSgTzhjLaEmyFfu4YUfT6-U_w8Xh2491QDmBnNBocr2ZdKbtjsZrscmCU0ZPi4icALGSvwH02scJ</recordid><startdate>19871101</startdate><enddate>19871101</enddate><creator>Fedida, D</creator><creator>Noble, D</creator><creator>Rankin, A C</creator><creator>Spindler, A J</creator><general>The Physiological Society</general><general>Blackwell</general><scope>IQODW</scope><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>7X8</scope><scope>5PM</scope></search><sort><creationdate>19871101</creationdate><title>The arrhythmogenic transient inward current iTI and related contraction in isolated guinea-pig ventricular myocytes</title><author>Fedida, D ; Noble, D ; Rankin, A C ; Spindler, A J</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5953-dd36d5192b6befed7b246b41c310ff97d2195b32635c7624932e23d6988201e13</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1987</creationdate><topic>Action Potentials - drug effects</topic><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Calcium - physiology</topic><topic>Cells, Cultured</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Guinea Pigs</topic><topic>Heart</topic><topic>Heart - physiology</topic><topic>In Vitro Techniques</topic><topic>Ion Channels - physiology</topic><topic>Myocardial Contraction</topic><topic>Potassium - pharmacology</topic><topic>Sodium - pharmacology</topic><topic>Strontium - pharmacology</topic><topic>Strophanthidin - pharmacology</topic><topic>Time Factors</topic><topic>Ventricular Function</topic><topic>Vertebrates: cardiovascular system</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Fedida, D</creatorcontrib><creatorcontrib>Noble, D</creatorcontrib><creatorcontrib>Rankin, A C</creatorcontrib><creatorcontrib>Spindler, A J</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>The Journal of physiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Fedida, D</au><au>Noble, D</au><au>Rankin, A C</au><au>Spindler, A J</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The arrhythmogenic transient inward current iTI and related contraction in isolated guinea-pig ventricular myocytes</atitle><jtitle>The Journal of physiology</jtitle><addtitle>J Physiol</addtitle><date>1987-11-01</date><risdate>1987</risdate><volume>392</volume><issue>1</issue><spage>523</spage><epage>542</epage><pages>523-542</pages><issn>0022-3751</issn><eissn>1469-7793</eissn><coden>JPHYA7</coden><abstract>1. The arrhythmogenic transient inward current, iTI, and contractions were recorded in isolated guinea-pig ventricular myocytes, after exposure to strophanthidin or low external K+ (0.5 mM), using a single-microelectrode voltage-clamp technique and an optical measure of contraction. 2. The inward current, iTI, and after-contraction occurred on repolarization after a depolarizing pre-pulse. Longer pre-pulses to more positive potentials increased the size and reduced the latency of iTI. Oscillatory currents and contractions also occurred during pulses to positive potentials. 3. The voltage dependence of iTI was studied by repolarizing to different potentials after a constant depolarizing pulse. Inward currents preceded after-contractions at all potentials. The iTI was maximal at about -50 mV, diminishing in magnitude at more negative and positive potentials. It remained inward at potentials up to +47 mV. The contraction exhibited a similar voltage dependence. The current-voltage relation varied in the same cell with longer exposure to glycosides. Thus, the voltage dependence of iTI reflected not only that of an underlying ionic mechanism but also the effects of potential on intracellular Ca2+ oscillations which trigger iTI. 4. Uniformity of internal Ca2+ transients was achieved by clamping to different potentials at the peak of an inward current. The iTI remained inward at positive potentials. An inward tail current, seen on repolarizing during iTI at the end of a depolarizing pre-pulse, progressively increased at negative potentials. This voltage dependence may be close to that of the Ca2+-activated inward current responsible for iTI. 5. Replacement of Na+ by Li+ initially increased the magnitude of iTI, but further exposure abolished the inward current, while the after-contractions continued to increase. The potential dependence of iTI was not affected by exposure to zero Na+. Replacement of Ca2+ by Sr2+ also abolished iTI and the after-contraction, but the main effect was to slow their occurrence. 6. The voltage dependence of the Ca2+-activated inward current in guinea-pig ventricular myocytes leads us to favour electrogenic Na-Ca exchange current as a major component of iTI, under our experimental conditions.</abstract><cop>Oxford</cop><pub>The Physiological Society</pub><pmid>2451728</pmid><doi>10.1113/jphysiol.1987.sp016795</doi><tpages>20</tpages><oa>free_for_read</oa></addata></record>
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subjects Action Potentials - drug effects
Animals
Biological and medical sciences
Calcium - physiology
Cells, Cultured
Fundamental and applied biological sciences. Psychology
Guinea Pigs
Heart
Heart - physiology
In Vitro Techniques
Ion Channels - physiology
Myocardial Contraction
Potassium - pharmacology
Sodium - pharmacology
Strontium - pharmacology
Strophanthidin - pharmacology
Time Factors
Ventricular Function
Vertebrates: cardiovascular system
title The arrhythmogenic transient inward current iTI and related contraction in isolated guinea-pig ventricular myocytes
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