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| Title: | STIMULATORY ACTION OF ANGIOTENSIN II ON IKS POTASSIUM CURRENT IN GUINEA-PIG ATRIAL CELLS | |
| DOI No: | 10.1142/9789812702234_0064 | |
| Source: | ADVANCES IN ELECTROCARDIOLOGY 2004 (pp 257-260) | |
| Author(s): | DIMITAR ZANKOV
Department of Cardiovascular and Respiratory Medicine, Shiga University of Medical Science, Otsu, Shiga 520-2192, Japan WEI-GUANG DING Department of Physiology, Shiga University of Medical Science, Otsu, Shiga 520-2192, Japan HIROSHI MATSUURA Department of Physiology, Shiga University of Medical Science, Otsu, Shiga 520-2192, Japan MINORU HORIE Department of Cardiovascular and Respiratory Medicine, Shiga University of Medical Science, Otsu, Shiga 520-2192, Japan |
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| Abstract: | Present study aimed to investigate the effect of angiotensin II (AT II) on the slowly activating delayed rectifier K+ current (IKs) in guinea-pig atrial myocytes, search for responsible intracellular pathway(s), and record action potential during AT1-receptor activation using whole-cell patch-clamp technique. Bath-administration of AT II increased IKs, amplitude with Kh 6.16 nM, which was significantly prevented by valsartan (1 μM) and mimicked by the specific AT1-agonist Sar-AT II. In cells loaded with GDPβS (2 mM) or compound 48/80 (100 μM) as well as pretreatment with the protein kinase C (PKC) inhibitors H-7 (10 μM) or BIS (200 nM) abolished IKs, potentiation extensively but it was not affected by intracellular perfusion of BAFTA (20 mM). No further enhancement of IKs was measured after applying PKC-activator (PMA, 100 - 300 nM). Sar-AT II (100 nM) shortened action potential duration (APD) at 50 and 90% of repolarization by 50.4±2.7% and 44.5±2.0%, respectively. Subsequently added valsartan (1 μM) partially reversed APD. It is concluded that AT II enhances IKs through activation of AT1-receptor coupled to G protein-PLC-PKC pathway and affects APD. | |
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