Epinephrine augments von Willebrand factor-dependent shear-induced platelet aggregation

Shinya Goto, Yasuo Ikeda, Mitsuru Murata, Makoto Handa, Eiichi Takahashi, Akira Yoshioka, Yoshihiro Fujimura, Mayumi Fukuyama, Shunnosuke Handa, Satoshi Ogawa

Research output: Contribution to journalArticle

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Abstract

Background. Shear-induced platelet aggregation (SIPA) is an important mechanism in thrombogenesis. von Willebrand factor (vWF) binding to platelet glycoprotein Ib (GP Ib) has been found to be crucial for platelet aggregation under the high shear force probably generated in stenosed coronary artery. The physiological significance of vWF-dependent SIPA has not been clarified. Methods and Results. Blood samples were collected from 23 normal volunteers. SIPA was continuously monitored using a modified cone-plate viscometer adapted for measuring the transmitted light intensity of the material. The effects of low concentrations of epinephrine, ADP, and collagen on SIPA under both low shear (12 dyne/cm2) and high shear (108 dyne/cm2) force were investigated. All agonists tested enhanced SIPA under low shear force, whereas only epinephrine augmented SIPA under high shear force. The maximum extents of SIPA under high shear force in the absence and presence of epinephrine (10 ng/ml) were 37.9±11.5% and 59.7±13.9%, respectively. The antagonist of the α2-adrenergic receptor yohimbine (1 μg/ml) antagonized the effects of epinephrine. The monoclonal antibody NMC-4 against vWF, which was shown to inhibit its binding to GP Ib, completely abolished SIPA under high shear force, even in the presence of epinephrine. However, this antibody only partially inhibited SIPA under low shear force. Conclusions. Our findings suggest that epinephrine is the agonist that enhances SIPA mediated by vWF through its specific receptor. This may be clinically important because occlusion of the coronary artery often occurs in stenosed atherosclerotic vessels under sympathetic stimulation.

Original languageEnglish
Pages (from-to)1859-1863
Number of pages5
JournalCirculation
Volume86
Issue number6
Publication statusPublished - 1992 Dec

Fingerprint

von Willebrand Factor
Platelet Aggregation
Epinephrine
Platelet Glycoprotein GPIb-IX Complex
Coronary Vessels
Platelet Membrane Glycoproteins
Adrenergic Antagonists
Yohimbine
Adenosine Diphosphate
Healthy Volunteers
Collagen
Monoclonal Antibodies
Light

Keywords

  • α-receptor
  • Epinephrine
  • Platelets
  • Von Willebrand factor

ASJC Scopus subject areas

  • Physiology
  • Cardiology and Cardiovascular Medicine

Cite this

Goto, S., Ikeda, Y., Murata, M., Handa, M., Takahashi, E., Yoshioka, A., ... Ogawa, S. (1992). Epinephrine augments von Willebrand factor-dependent shear-induced platelet aggregation. Circulation, 86(6), 1859-1863.

Epinephrine augments von Willebrand factor-dependent shear-induced platelet aggregation. / Goto, Shinya; Ikeda, Yasuo; Murata, Mitsuru; Handa, Makoto; Takahashi, Eiichi; Yoshioka, Akira; Fujimura, Yoshihiro; Fukuyama, Mayumi; Handa, Shunnosuke; Ogawa, Satoshi.

In: Circulation, Vol. 86, No. 6, 12.1992, p. 1859-1863.

Research output: Contribution to journalArticle

Goto, S, Ikeda, Y, Murata, M, Handa, M, Takahashi, E, Yoshioka, A, Fujimura, Y, Fukuyama, M, Handa, S & Ogawa, S 1992, 'Epinephrine augments von Willebrand factor-dependent shear-induced platelet aggregation', Circulation, vol. 86, no. 6, pp. 1859-1863.
Goto S, Ikeda Y, Murata M, Handa M, Takahashi E, Yoshioka A et al. Epinephrine augments von Willebrand factor-dependent shear-induced platelet aggregation. Circulation. 1992 Dec;86(6):1859-1863.
Goto, Shinya ; Ikeda, Yasuo ; Murata, Mitsuru ; Handa, Makoto ; Takahashi, Eiichi ; Yoshioka, Akira ; Fujimura, Yoshihiro ; Fukuyama, Mayumi ; Handa, Shunnosuke ; Ogawa, Satoshi. / Epinephrine augments von Willebrand factor-dependent shear-induced platelet aggregation. In: Circulation. 1992 ; Vol. 86, No. 6. pp. 1859-1863.
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AU - Goto, Shinya

AU - Ikeda, Yasuo

AU - Murata, Mitsuru

AU - Handa, Makoto

AU - Takahashi, Eiichi

AU - Yoshioka, Akira

AU - Fujimura, Yoshihiro

AU - Fukuyama, Mayumi

AU - Handa, Shunnosuke

AU - Ogawa, Satoshi

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N2 - Background. Shear-induced platelet aggregation (SIPA) is an important mechanism in thrombogenesis. von Willebrand factor (vWF) binding to platelet glycoprotein Ib (GP Ib) has been found to be crucial for platelet aggregation under the high shear force probably generated in stenosed coronary artery. The physiological significance of vWF-dependent SIPA has not been clarified. Methods and Results. Blood samples were collected from 23 normal volunteers. SIPA was continuously monitored using a modified cone-plate viscometer adapted for measuring the transmitted light intensity of the material. The effects of low concentrations of epinephrine, ADP, and collagen on SIPA under both low shear (12 dyne/cm2) and high shear (108 dyne/cm2) force were investigated. All agonists tested enhanced SIPA under low shear force, whereas only epinephrine augmented SIPA under high shear force. The maximum extents of SIPA under high shear force in the absence and presence of epinephrine (10 ng/ml) were 37.9±11.5% and 59.7±13.9%, respectively. The antagonist of the α2-adrenergic receptor yohimbine (1 μg/ml) antagonized the effects of epinephrine. The monoclonal antibody NMC-4 against vWF, which was shown to inhibit its binding to GP Ib, completely abolished SIPA under high shear force, even in the presence of epinephrine. However, this antibody only partially inhibited SIPA under low shear force. Conclusions. Our findings suggest that epinephrine is the agonist that enhances SIPA mediated by vWF through its specific receptor. This may be clinically important because occlusion of the coronary artery often occurs in stenosed atherosclerotic vessels under sympathetic stimulation.

AB - Background. Shear-induced platelet aggregation (SIPA) is an important mechanism in thrombogenesis. von Willebrand factor (vWF) binding to platelet glycoprotein Ib (GP Ib) has been found to be crucial for platelet aggregation under the high shear force probably generated in stenosed coronary artery. The physiological significance of vWF-dependent SIPA has not been clarified. Methods and Results. Blood samples were collected from 23 normal volunteers. SIPA was continuously monitored using a modified cone-plate viscometer adapted for measuring the transmitted light intensity of the material. The effects of low concentrations of epinephrine, ADP, and collagen on SIPA under both low shear (12 dyne/cm2) and high shear (108 dyne/cm2) force were investigated. All agonists tested enhanced SIPA under low shear force, whereas only epinephrine augmented SIPA under high shear force. The maximum extents of SIPA under high shear force in the absence and presence of epinephrine (10 ng/ml) were 37.9±11.5% and 59.7±13.9%, respectively. The antagonist of the α2-adrenergic receptor yohimbine (1 μg/ml) antagonized the effects of epinephrine. The monoclonal antibody NMC-4 against vWF, which was shown to inhibit its binding to GP Ib, completely abolished SIPA under high shear force, even in the presence of epinephrine. However, this antibody only partially inhibited SIPA under low shear force. Conclusions. Our findings suggest that epinephrine is the agonist that enhances SIPA mediated by vWF through its specific receptor. This may be clinically important because occlusion of the coronary artery often occurs in stenosed atherosclerotic vessels under sympathetic stimulation.

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