Are B-type Ca2+ Channels of Cardiac Myocytes Akin to the Passive Ion Channel in the Plasma Membrane Ca2+ Pump?

Are B-type Ca2+ Channels of Cardiac Myocytes Akin to the Passive Ion Channel in the Plasma... The present study demonstrates that B-type Ca2+ channels observed in rat ventricular myocytes markedly reacted to agents known to affect the ion-motive plasma membrane Ca2+-ATPase (PMCA) pump. Chlorpromazine (CPZ)-activated B-type Ca2+ channels were completely blocked by internal application of PMCA pump inhibitors, namely La3+ (100 μm), eosin (10 μm) and AIF3 (100 μm). Calmodulin (50 U/ml), the main endogenous positive regulator of PMCA, was unable to activate but significantly reduced CPZ-activated B-type channel activity. In the same manner, ATP (1 and 4 mm), the main energizing substrate of PMCA, was able to reversibly and significantly reduce this activity in a dose-dependent manner. Interestingly, anti-PMCA antibody 5F10, but not anti-Na/K ATPase antibody (used as a negative control) induced a marked Ba2+-conducting channel activity that shared the same characteristics with that of CPZ-activated B-type channels. 5F10-Activated channels were mostly selective towards Ba2+, mainly had three observed conductance levels (23, 47 and 85 pS), were observed with a frequency of about 1 out of 5 membrane patches and were completely blocked by 10 μm eosin. These results suggest that B-type Ca2+ channels are some form of the PMCA pump. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png The Journal of Membrane Biology Springer Journals

Are B-type Ca2+ Channels of Cardiac Myocytes Akin to the Passive Ion Channel in the Plasma Membrane Ca2+ Pump?

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Publisher
Springer-Verlag
Copyright
Copyright © Inc. by 2001 Springer-Verlag New York
Subject
Life Sciences; Biochemistry, general; Human Physiology
ISSN
0022-2631
eISSN
1432-1424
D.O.I.
10.1007/s002320010035
Publisher site
See Article on Publisher Site

Abstract

The present study demonstrates that B-type Ca2+ channels observed in rat ventricular myocytes markedly reacted to agents known to affect the ion-motive plasma membrane Ca2+-ATPase (PMCA) pump. Chlorpromazine (CPZ)-activated B-type Ca2+ channels were completely blocked by internal application of PMCA pump inhibitors, namely La3+ (100 μm), eosin (10 μm) and AIF3 (100 μm). Calmodulin (50 U/ml), the main endogenous positive regulator of PMCA, was unable to activate but significantly reduced CPZ-activated B-type channel activity. In the same manner, ATP (1 and 4 mm), the main energizing substrate of PMCA, was able to reversibly and significantly reduce this activity in a dose-dependent manner. Interestingly, anti-PMCA antibody 5F10, but not anti-Na/K ATPase antibody (used as a negative control) induced a marked Ba2+-conducting channel activity that shared the same characteristics with that of CPZ-activated B-type channels. 5F10-Activated channels were mostly selective towards Ba2+, mainly had three observed conductance levels (23, 47 and 85 pS), were observed with a frequency of about 1 out of 5 membrane patches and were completely blocked by 10 μm eosin. These results suggest that B-type Ca2+ channels are some form of the PMCA pump.

Journal

The Journal of Membrane BiologySpringer Journals

Published: Jan 1, 2001

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