Abstract
Many receptors coupled to inhibitory Go/Gi-type G proteins often also produce stimulatory signals like Ca2+ mobilisation. When expressed in CHO cells the alpha2-adrenoceptor subtypes alpha2A, alpha2B and alpkha2C mobilised Ca2+. These responses were strongly reduced by the P2Y-purinoceptor antagonist suramin. A large proportion of the total pool of purine nucleotides was found extracellularly. Removal of extracellular nucleotides with apyrase or by constant perfusion had a similar effect as suramin. These treatments did not affect the alpha2-adrenoceptor-mediated inhibition of cAMP production. This indicates that cells may be primed or their signaling pathways redirected towards Ca2+ mobilisation by 'autocrine' release of nucleotides.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Adenosine Triphosphate / pharmacology*
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Adenosine Triphosphate / physiology
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Adrenergic alpha-Agonists / pharmacology
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Animals
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Apyrase / pharmacology
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CHO Cells
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Calcium / metabolism*
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Calcium-Transporting ATPases / antagonists & inhibitors
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Cricetinae
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Cyclic AMP / metabolism
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Enzyme Inhibitors / pharmacology
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Norepinephrine / pharmacology
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Purinergic P2 Receptor Antagonists
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Receptors, Adrenergic, alpha-2 / physiology*
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Signal Transduction / physiology*
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Suramin / pharmacology
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Thapsigargin / pharmacology
Substances
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Adrenergic alpha-Agonists
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Enzyme Inhibitors
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Purinergic P2 Receptor Antagonists
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Receptors, Adrenergic, alpha-2
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Suramin
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Thapsigargin
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Adenosine Triphosphate
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Cyclic AMP
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Apyrase
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Calcium-Transporting ATPases
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Calcium
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Norepinephrine