Abstract
The effects of heparin on the release of intracellular Ca2+, assessed by tension development in saponin-permeabilized rabbit main pulmonary artery, were determined. Heparin inhibited (IC50 = 5 micrograms/ml) inositol 1,4,5-trisphosphate (InsP3)-induced, but not caffeine-induced, Ca2+ release. The initial (InsP3-dependent) component of GTP gamma S-induced Ca2+-release was also inhibited by heparin, but the InsP3-independent component was resistant to both heparin and procaine. These results support the existence of a G protein activated mechanism of Ca2+ release that is not mediated by InsP3 or by Ca2+-induced Ca2+ release.
Publication types
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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Animals
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Caffeine / pharmacology
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Calcium / metabolism*
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GTP-Binding Proteins / physiology*
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Guanosine 5'-O-(3-Thiotriphosphate)
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Guanosine Triphosphate / analogs & derivatives
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Guanosine Triphosphate / pharmacology
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Heparin / pharmacology*
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In Vitro Techniques
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Inositol 1,4,5-Trisphosphate
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Inositol Phosphates / physiology*
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Muscle Contraction / drug effects
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Muscle, Smooth, Vascular / physiology*
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Procaine / pharmacology
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Rabbits
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Sugar Phosphates / physiology*
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Thionucleotides / pharmacology
Substances
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Inositol Phosphates
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Sugar Phosphates
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Thionucleotides
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Guanosine 5'-O-(3-Thiotriphosphate)
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Caffeine
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Procaine
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Inositol 1,4,5-Trisphosphate
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Guanosine Triphosphate
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Heparin
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GTP-Binding Proteins
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Calcium