scholarly journals Noradrenaline up-regulates volume-regulated chloride current by PKA-independent cAMP/exchange protein activated by cAMP pathway in human atrial myocytes

2018 ◽  
Vol 175 (16) ◽  
pp. 3422-3432 ◽  
Author(s):  
Guo-Sheng Xiao ◽  
Yan-Hui Zhang ◽  
Yan Wang ◽  
Hai-Ying Sun ◽  
Clive M Baumgarten ◽  
...  
Keyword(s):  
Chloride Current ◽  
Atrial Myocytes ◽  
Human Atrial Myocytes ◽  
Camp Pathway ◽  
Exchange Protein

scholarly journals Differential Effects of Tyrosine Kinase Inhibitors on Volume-sensitive Chloride Current in Human Atrial Myocytes

2004 ◽  
Vol 123 (4) ◽  
pp. 427-439 ◽  
Author(s):  
Xin-Ling Du ◽  
Zhan Gao ◽  
Chu-Pak Lau ◽  
Shui-Wah Chiu ◽  
Hung-Fat Tse ◽  
...  
Keyword(s):  
Tyrosine Kinase ◽  
Broad Spectrum ◽  
Kinase Inhibitor ◽  
Chloride Current ◽  
Disulfonic Acid ◽  
Dependent Manner ◽  
Atrial Myocytes ◽  
Concentration Dependent Manner ◽  
Human Atrial Myocytes ◽  
Protein Tyrosine

To determine whether protein tyrosine kinase (PTK) modulates volume-sensitive chloride current (ICl.vol) in human atrial myocytes and to identify the PTKs involved, we studied the effects of broad-spectrum and selective PTK inhibitors and the protein tyrosine phosphatase (PTP) inhibitor orthovanadate (VO4−3). ICl.vol evoked by hyposmotic bath solution (0.6-times isosmotic, 0.6T) was enhanced by genistein, a broad-spectrum PTK inhibitor, in a concentration-dependent manner (EC50 = 22.4 μM); 100 μM genistein stimulated ICl.vol by 122.4 ± 10.6%. The genistein-stimulated current was inhibited by DIDS (4,4′-diisothiocyanostilbene-2,2′-disulfonic acid, 150 μM) and tamoxifen (20 μM), blockers of ICl.vol. Moreover, the current augmented by genistein was volume dependent; it was abolished by hyperosmotic shrinkage in 1.4T, and genistein did not activate Cl− current in 1T. In contrast to the stimulatory effects of genistein, 100 μM tyrphostin A23 (AG 18) and A25 (AG 82) inhibited ICl.vol by 38.2 ± 4.9% and 40.9 ± 3.4%, respectively. The inactive analogs, daidzein and tyrphostin A63 (AG 43), did not alter ICl.vol. In addition, the PTP inhibitor VO4−3 (1 mM) reduced ICl.vol by 53.5 ± 4.5% (IC50 = 249.6 μM). Pretreatment with VO4−3 antagonized genistein-induced augmentation and A23- or A25-induced suppression of ICl.vol. Furthermore, the selective Src-family PTK inhibitor PP2 (5 μM) stimulated ICl.vol, mimicking genistein, whereas the selective EGFR (ErbB-1) kinase inhibitor tyrphostin B56 (AG 556, 25 μM) reduced ICl.vol, mimicking A23 and A25. The effects of both PP2 and B56 also were substantially antagonized by pretreatment with VO4−3. The results suggest that ICl.vol is regulated in part by the balance between PTK and PTP activity. Regulation is complex, however. Src and EGFR kinases, distinct soluble and receptor-mediated PTK families, have opposing effects on ICl.vol, and multiple target proteins are likely to be involved.

scholarly journals Chloride current in human atrial myocytes.

1995 ◽  
Vol 15 (3) ◽  
pp. 211-215
Author(s):  
Nobuhisa Hagiwara ◽  
Rieko Sakai ◽  
Naoki Matsuda ◽  
Hiroshi Kasanuki ◽  
Saichi Hosoda ◽  
...  
Keyword(s):  
Chloride Current ◽  
Atrial Myocytes ◽  
Human Atrial Myocytes

scholarly journals Sarcoplasmic reticulum and L-type Ca2+channel activity regulate the beat-to-beat stability of calcium handling in human atrial myocytes

2011 ◽  
Vol 589 (13) ◽  
pp. 3247-3262 ◽  
Author(s):  
Anna Llach ◽  
Cristina E. Molina ◽  
Jacqueline Fernandes ◽  
Josep Padró ◽  
Juan Cinca ◽  
...  
Keyword(s):  
Sarcoplasmic Reticulum ◽  
Calcium Handling ◽  
Channel Activity ◽  
Atrial Myocytes ◽  
Human Atrial Myocytes
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