Effect of heparin and dextran sulfate on cationic polypeptide-induced endothelial dysfunction in isolated canine basilar artery

H. Kinoshita, Zvonimir S Katusic

Research output: Contribution to journalArticle

Abstract

Cationic polypeptides can be released by activated leukocytes. Previous studies indicated that cationic polypeptides cause endothelial dysfunction by inhibiting endothelium-dependent relaxations. The present study was designed to determine if, in cerebral arteries, anionic molecules heparin and dextran sulfate may prevent endothelial dysfunction induced by synthetic cationic polypeptides poly-L-arginine (PLA; 10-6M) and poly-L-lysine (PLL; 10-6 M). Rings of canine basilar arteries with endothelium were suspended in organ chambers for isometric tension recordings. All experiments were performed in arteries treated with indomethacin (10-5M). In arteries exposed to PLA (10-6M) or PLL (10-6M), endotheliumdependent relaxations to bradykinin (10-10 to 10-6M) were abolished. Pretreatment with heparin (50 U/ml) or dextran sulfate (200 ug/ml) restored relaxations to bradykinin. These results suggest that in cerebral arteries negatively charged molecules prevent endothelial dysfunction induced by cationic polypeptides via charge dependent mechanism. We speculate that negatively charged molecules can protect cerebral endothelial cells from functional damage during inflammatory vascular diseases.

Original languageEnglish (US)
JournalFASEB Journal
Volume10
Issue number3
StatePublished - 1996

Fingerprint

Dextran Sulfate
Basilar Artery
heparin
dextran
arteries
Heparin
Canidae
polypeptides
sulfates
Peptides
Cerebral Arteries
dogs
Bradykinin
Phase locked loops
bradykinin
Molecules
Endothelium
endothelium
Arteries
Endothelial cells

ASJC Scopus subject areas

  • Agricultural and Biological Sciences (miscellaneous)
  • Biochemistry, Genetics and Molecular Biology(all)
  • Biochemistry
  • Cell Biology

Cite this

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abstract = "Cationic polypeptides can be released by activated leukocytes. Previous studies indicated that cationic polypeptides cause endothelial dysfunction by inhibiting endothelium-dependent relaxations. The present study was designed to determine if, in cerebral arteries, anionic molecules heparin and dextran sulfate may prevent endothelial dysfunction induced by synthetic cationic polypeptides poly-L-arginine (PLA; 10-6M) and poly-L-lysine (PLL; 10-6 M). Rings of canine basilar arteries with endothelium were suspended in organ chambers for isometric tension recordings. All experiments were performed in arteries treated with indomethacin (10-5M). In arteries exposed to PLA (10-6M) or PLL (10-6M), endotheliumdependent relaxations to bradykinin (10-10 to 10-6M) were abolished. Pretreatment with heparin (50 U/ml) or dextran sulfate (200 ug/ml) restored relaxations to bradykinin. These results suggest that in cerebral arteries negatively charged molecules prevent endothelial dysfunction induced by cationic polypeptides via charge dependent mechanism. We speculate that negatively charged molecules can protect cerebral endothelial cells from functional damage during inflammatory vascular diseases.",
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AB - Cationic polypeptides can be released by activated leukocytes. Previous studies indicated that cationic polypeptides cause endothelial dysfunction by inhibiting endothelium-dependent relaxations. The present study was designed to determine if, in cerebral arteries, anionic molecules heparin and dextran sulfate may prevent endothelial dysfunction induced by synthetic cationic polypeptides poly-L-arginine (PLA; 10-6M) and poly-L-lysine (PLL; 10-6 M). Rings of canine basilar arteries with endothelium were suspended in organ chambers for isometric tension recordings. All experiments were performed in arteries treated with indomethacin (10-5M). In arteries exposed to PLA (10-6M) or PLL (10-6M), endotheliumdependent relaxations to bradykinin (10-10 to 10-6M) were abolished. Pretreatment with heparin (50 U/ml) or dextran sulfate (200 ug/ml) restored relaxations to bradykinin. These results suggest that in cerebral arteries negatively charged molecules prevent endothelial dysfunction induced by cationic polypeptides via charge dependent mechanism. We speculate that negatively charged molecules can protect cerebral endothelial cells from functional damage during inflammatory vascular diseases.

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