Abstract
Adrenomedullin is a biologically active peptide released from the vascular wall, which increases blood flow through its vasorelaxant effects and prevents platelet activation by stimulation of nitric oxide synthesis. The present study demonstrates that activated platelets suppress adrenomedullin secretion from vascular endothelial cells by releasing a factor that was identified as transforming growth factor (TGF)-beta1. Adrenomedullin levels were reduced by up to 40% and this effect was completely abrogated by the addition of latency-associated protein (LAP) or TGF-beta1-neutralizing antibody. Inhibition of adrenomedullin secretion in response to platelet aggregation may be an important mechanism in the induction of hemostasis.
MeSH terms
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Adrenomedullin
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Animals
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Antibodies / pharmacology
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Blood Platelets / metabolism*
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Cattle
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Culture Media, Conditioned / chemistry
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Culture Media, Conditioned / pharmacology
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Dose-Response Relationship, Drug
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Endothelium, Vascular / cytology
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Endothelium, Vascular / drug effects
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Endothelium, Vascular / metabolism
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Humans
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Peptide Fragments / immunology
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Peptide Fragments / pharmacology
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Peptides / drug effects
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Peptides / metabolism*
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Peptides / pharmacology
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Platelet Activation / drug effects
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Platelet Aggregation / drug effects
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Protein Precursors / immunology
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Protein Precursors / pharmacology
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Recombinant Proteins / pharmacology
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Thrombin / pharmacology
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Transforming Growth Factor beta / immunology
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Transforming Growth Factor beta / pharmacology
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Transforming Growth Factor beta1
Substances
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Antibodies
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Culture Media, Conditioned
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Peptide Fragments
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Peptides
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Protein Precursors
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Recombinant Proteins
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TGFB1 protein, human
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Transforming Growth Factor beta
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Transforming Growth Factor beta1
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Adrenomedullin
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Thrombin