Abstract
The role of endothelium-derived nitric oxide (NO) to cause smooth muscle phospholamban (PLB) phosphorylation was studied in the isolated perfused rat aorta precontracted with norepinephrine using a back-phosphorylation technique. NO-induced relaxation was associated with increased PLB-phosphorylation while norepinephrine as such was ineffective. Removal of endothelium significantly reduced PLB-phosphorylation in indomethacin treated vessels. Stimulation of NO-formation by ATP augmented PLB-phosphorylation in intact vessels but was ineffective in denuded aortas. The results indicate that PLB-phosphorylation of vascular smooth muscle plays an important role in mediating NO-dependent relaxation by enhancing Ca(++)-uptake into sarcoplasmic reticulum.
MeSH terms
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Adenosine Triphosphate / metabolism
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Animals
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Aorta / drug effects
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Aorta / physiology
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Calcium-Binding Proteins / metabolism
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Calcium-Binding Proteins / physiology*
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Endothelium, Vascular / metabolism
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Endothelium, Vascular / physiology
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Muscle Contraction / drug effects
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Muscle Relaxation / drug effects
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Muscle Relaxation / physiology*
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Muscle, Smooth, Vascular / drug effects
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Muscle, Smooth, Vascular / metabolism
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Muscle, Smooth, Vascular / physiology*
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Nitric Oxide / biosynthesis
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Nitric Oxide / metabolism*
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Nitric Oxide / pharmacology
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Nitric Oxide / physiology*
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Norepinephrine / pharmacology
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Phosphorus Radioisotopes
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Phosphorylation
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Rats
Substances
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Calcium-Binding Proteins
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Phosphorus Radioisotopes
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phospholamban
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Nitric Oxide
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Adenosine Triphosphate
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Norepinephrine