Hirudin (Desulfated, 54-65) causes contracton of canine coronary arteries which is attenuated by calcium-channel blockers

P. Sorajja, D. G. Cable, Hartzell V Schaff

Research output: Contribution to journalArticle

Abstract

Background: Hirudin is a novel antithrombin agent with potent anticoagulatory properties. Previous studies have demonstrated that hirudin stimulates the release of nitric oxide in porcine pulmonary arteries. We investigated hirudin for its direct effects on coronary arteries. Methods and Results: Canine coronary arteries were mounted in organ chambers and precontracted with prostaglandin F2 α(2x10-6M). In arteries with intact endothelium, hirudin (10-1 to 10-6M) increased vascular tension 33.6±9.0% above baseline tension (n=10, p<0.05 ANOVA). In arteries denuded of endothelium, hirudin increased vascular tension 31.8±11.2% above baseline tension (n=8, p<0.05),demonstrating that the hirudin-mediated contractions were endothelium independent. Pretreatment of the coronary arteries with either verapamil (10-4M) or nifedipine (10-4M) for one hour attenuated hirudin-mediated vascular contractions. Whereas control arteries contracted 26.4±10.3% above baseline tension, hirudin administration increased vascular tension 3.8±7.0% above baseline tension in arteries pretreated with verapamil (n=6, p<0.05 vs. control) and 6.2±12.4% above baseline tension in arteries pretreated with nifedipine(n=6,p<0.05). Conclusions: The present study demonstrates that hirudin induces endothelium-independent contractions of canine coronary arteries. Attenuation of these contractions by calcium-channel blockers suggests a possible mechanism by which hirudin mediates coronary artery constriction.

Original languageEnglish (US)
JournalFASEB Journal
Volume12
Issue number5
StatePublished - Mar 20 1998

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Hirudins
calcium channel blockers
Calcium Channel Blockers
coronary vessels
arteries
Canidae
Coronary Vessels
endothelium
blood vessels
dogs
verapamil
Arteries
Endothelium
Blood Vessels
pulmonary artery
Nifedipine
Verapamil
prostaglandins
nitric oxide
pretreatment

ASJC Scopus subject areas

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

Cite this

Hirudin (Desulfated, 54-65) causes contracton of canine coronary arteries which is attenuated by calcium-channel blockers. / Sorajja, P.; Cable, D. G.; Schaff, Hartzell V.

In: FASEB Journal, Vol. 12, No. 5, 20.03.1998.

Research output: Contribution to journalArticle

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abstract = "Background: Hirudin is a novel antithrombin agent with potent anticoagulatory properties. Previous studies have demonstrated that hirudin stimulates the release of nitric oxide in porcine pulmonary arteries. We investigated hirudin for its direct effects on coronary arteries. Methods and Results: Canine coronary arteries were mounted in organ chambers and precontracted with prostaglandin F2 α(2x10-6M). In arteries with intact endothelium, hirudin (10-1 to 10-6M) increased vascular tension 33.6±9.0{\%} above baseline tension (n=10, p<0.05 ANOVA). In arteries denuded of endothelium, hirudin increased vascular tension 31.8±11.2{\%} above baseline tension (n=8, p<0.05),demonstrating that the hirudin-mediated contractions were endothelium independent. Pretreatment of the coronary arteries with either verapamil (10-4M) or nifedipine (10-4M) for one hour attenuated hirudin-mediated vascular contractions. Whereas control arteries contracted 26.4±10.3{\%} above baseline tension, hirudin administration increased vascular tension 3.8±7.0{\%} above baseline tension in arteries pretreated with verapamil (n=6, p<0.05 vs. control) and 6.2±12.4{\%} above baseline tension in arteries pretreated with nifedipine(n=6,p<0.05). Conclusions: The present study demonstrates that hirudin induces endothelium-independent contractions of canine coronary arteries. Attenuation of these contractions by calcium-channel blockers suggests a possible mechanism by which hirudin mediates coronary artery constriction.",
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