Effects of exogenous phosphatidic acid on calcium current of ventricular myocytes

Wen Jie Zhang, Jing Yan Ge, Chun Yan Zhao, Xue Xin Zhang, Shu Zhan, Gou Gan Zhong

Research output: Contribution to journalArticle

Abstract

Objective: To study the effects of exogenous phosphatidic acid (PA) on calcium current of ventricular myocytes. Methods: The Langendorff perfu sion method was used to isolate the ventricular myocytes of guinea pigs and the ventricular myocytes of guinea pigs were randomly divided into control groups, three dosage groups of PA 0.01, 0.1 and 1.0 μmol · L-1 and group of PTX 0. 1 mg · L-1 plus PA 1. 0 μmol · L-1 and group of H-7 2 μmol · L-1 plus PA 1. 0 μmol · L-1. The whole cell voltage clamp technique was used to record the calcium current of isolated ventricular myocytes of guinea pigs. Results: 0.01, 0.1 and 1.0 μmol · L-1 P A enhanced the calcium current from (288.70 ± 28.33) pA, (290.83 ± 25.12) pA and (279.54 ± 31.22) pA before administration to (304.10±28.31) pA (P>0.05), (349.80±30.13) pA (P<0.01) and (388.10±28.12) pA (P<0.001) after administration. The effects of PA on the calcium current was blocked by PTX (a G protein-coupled receptor blocking agent) and H-7 (a PKC blocking agent). Conclusion: PA can promote the opening of calcium chan nels of the ventricular myocytes by the pathway of membrane receptor-G protein-PKC in a dose-dependent manner.

Original languageEnglish (US)
Pages (from-to)422-424
Number of pages3
JournalJournal of Jilin University Medicine Edition
Volume32
Issue number3
StatePublished - May 1 2006

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Phosphatidic Acids
Muscle Cells
Calcium
1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine
Guinea Pigs
Patch-Clamp Techniques
G-Protein-Coupled Receptors
GTP-Binding Proteins
Control Groups
Membranes

All Science Journal Classification (ASJC) codes

  • Pharmacology

Cite this

Zhang, Wen Jie ; Ge, Jing Yan ; Zhao, Chun Yan ; Zhang, Xue Xin ; Zhan, Shu ; Zhong, Gou Gan. / Effects of exogenous phosphatidic acid on calcium current of ventricular myocytes. In: Journal of Jilin University Medicine Edition. 2006 ; Vol. 32, No. 3. pp. 422-424.
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abstract = "Objective: To study the effects of exogenous phosphatidic acid (PA) on calcium current of ventricular myocytes. Methods: The Langendorff perfu sion method was used to isolate the ventricular myocytes of guinea pigs and the ventricular myocytes of guinea pigs were randomly divided into control groups, three dosage groups of PA 0.01, 0.1 and 1.0 μmol · L-1 and group of PTX 0. 1 mg · L-1 plus PA 1. 0 μmol · L-1 and group of H-7 2 μmol · L-1 plus PA 1. 0 μmol · L-1. The whole cell voltage clamp technique was used to record the calcium current of isolated ventricular myocytes of guinea pigs. Results: 0.01, 0.1 and 1.0 μmol · L-1 P A enhanced the calcium current from (288.70 ± 28.33) pA, (290.83 ± 25.12) pA and (279.54 ± 31.22) pA before administration to (304.10±28.31) pA (P>0.05), (349.80±30.13) pA (P<0.01) and (388.10±28.12) pA (P<0.001) after administration. The effects of PA on the calcium current was blocked by PTX (a G protein-coupled receptor blocking agent) and H-7 (a PKC blocking agent). Conclusion: PA can promote the opening of calcium chan nels of the ventricular myocytes by the pathway of membrane receptor-G protein-PKC in a dose-dependent manner.",
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Effects of exogenous phosphatidic acid on calcium current of ventricular myocytes. / Zhang, Wen Jie; Ge, Jing Yan; Zhao, Chun Yan; Zhang, Xue Xin; Zhan, Shu; Zhong, Gou Gan.

In: Journal of Jilin University Medicine Edition, Vol. 32, No. 3, 01.05.2006, p. 422-424.

Research output: Contribution to journalArticle

TY - JOUR

T1 - Effects of exogenous phosphatidic acid on calcium current of ventricular myocytes

AU - Zhang, Wen Jie

AU - Ge, Jing Yan

AU - Zhao, Chun Yan

AU - Zhang, Xue Xin

AU - Zhan, Shu

AU - Zhong, Gou Gan

PY - 2006/5/1

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N2 - Objective: To study the effects of exogenous phosphatidic acid (PA) on calcium current of ventricular myocytes. Methods: The Langendorff perfu sion method was used to isolate the ventricular myocytes of guinea pigs and the ventricular myocytes of guinea pigs were randomly divided into control groups, three dosage groups of PA 0.01, 0.1 and 1.0 μmol · L-1 and group of PTX 0. 1 mg · L-1 plus PA 1. 0 μmol · L-1 and group of H-7 2 μmol · L-1 plus PA 1. 0 μmol · L-1. The whole cell voltage clamp technique was used to record the calcium current of isolated ventricular myocytes of guinea pigs. Results: 0.01, 0.1 and 1.0 μmol · L-1 P A enhanced the calcium current from (288.70 ± 28.33) pA, (290.83 ± 25.12) pA and (279.54 ± 31.22) pA before administration to (304.10±28.31) pA (P>0.05), (349.80±30.13) pA (P<0.01) and (388.10±28.12) pA (P<0.001) after administration. The effects of PA on the calcium current was blocked by PTX (a G protein-coupled receptor blocking agent) and H-7 (a PKC blocking agent). Conclusion: PA can promote the opening of calcium chan nels of the ventricular myocytes by the pathway of membrane receptor-G protein-PKC in a dose-dependent manner.

AB - Objective: To study the effects of exogenous phosphatidic acid (PA) on calcium current of ventricular myocytes. Methods: The Langendorff perfu sion method was used to isolate the ventricular myocytes of guinea pigs and the ventricular myocytes of guinea pigs were randomly divided into control groups, three dosage groups of PA 0.01, 0.1 and 1.0 μmol · L-1 and group of PTX 0. 1 mg · L-1 plus PA 1. 0 μmol · L-1 and group of H-7 2 μmol · L-1 plus PA 1. 0 μmol · L-1. The whole cell voltage clamp technique was used to record the calcium current of isolated ventricular myocytes of guinea pigs. Results: 0.01, 0.1 and 1.0 μmol · L-1 P A enhanced the calcium current from (288.70 ± 28.33) pA, (290.83 ± 25.12) pA and (279.54 ± 31.22) pA before administration to (304.10±28.31) pA (P>0.05), (349.80±30.13) pA (P<0.01) and (388.10±28.12) pA (P<0.001) after administration. The effects of PA on the calcium current was blocked by PTX (a G protein-coupled receptor blocking agent) and H-7 (a PKC blocking agent). Conclusion: PA can promote the opening of calcium chan nels of the ventricular myocytes by the pathway of membrane receptor-G protein-PKC in a dose-dependent manner.

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