Journal article
Stimulation of cardiac L-type calcium channels by extracellular ATP
American Journal of Physiology: Cell Physiology, v 280(5), pp C1107-C1113
01 May 2001
PMID: 11287323
Featured in Collection : UN Sustainable Development Goals @ Drexel
Abstract
The co-release of ATP with norepinephrine from sympathetic nerve terminals in the heart may augment adrenergic stimulation of cardiac Ca
2+
channel activity. To test for a possible direct effect of extracellular ATP on L-type Ca
2+
channels, single channels were reconstituted from porcine sarcolemma into planar lipid bilayers so that intracellular signaling pathways could be controlled. Extracellular ATP (2–100 μM) increased the open probability of the reconstituted channels, with a maximal increase of ∼2.6-fold and an EC
50
of 3.9 μM. The increase in open probability was due to an increase in channel availability and a decrease in channel inactivation rate. Other nucleotides displayed a rank order of effectiveness of ATP > α,β-methylene-ATP > 2-methylthio-ATP > UTP > adenosine 5′- O-(3-thiotriphosphate) >> ADP; adenosine had no effect. Several antagonists of P2 receptors had no impact on the ATP-dependent increase in open probability, indicating that receptor activation was not required. These results suggest that extracellular ATP and other nucleotides can stimulate the activity of cardiac L-type Ca
2+
channels via a direct interaction with the channels.
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Details
- Title
- Stimulation of cardiac L-type calcium channels by extracellular ATP
- Creators
- Qi-Yi Liu - University of North Carolina at Chapel HillRobert L. Rosenberg - University of North Carolina at Chapel Hill
- Publication Details
- American Journal of Physiology: Cell Physiology, v 280(5), pp C1107-C1113
- Publisher
- American Physiological Society (APS)
- Resource Type
- Journal article
- Language
- English
- Academic Unit
- Pharmacology and Physiology
- Web of Science ID
- WOS:000168221100010
- Scopus ID
- 2-s2.0-0035011482
- Other Identifier
- 991021902518104721
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- Web of Science research areas
- Cell Biology
- Physiology