On the role of calcium in the acute release of tissue-type plasminogen activator and von Willebrand factor from the rat perfused hindleg region
article
The involvement of calcium in the release of tissue-type plasminogen activator (t-PA) and von Willebrand Factor (vWF) from vascular endothelial cells was studied ex vivo using a rat hindleg perfusion system. By adding either platelet-activating factor or bradykinin to the perfusing Tyrode solution, a rapid release of t-PA and vWF was induced. Extracellular calcium was required for the acute release of both glycoproteins as this release was totally abolished in the presence of EGTA. The calcium ionophore A-23187 induced (Ca-dependently) the release of both proteins, suggesting that Ca-influx was also sufficient to induce release. The absence of an effect of the calcium L-type channel blockers, verapamil and diltiazem, and of the calcium channel agonist BAY K-8644, suggested that endothelial voltage-operated calcium channels were not involved in release. Trifluoperazine, a calmodulin antagonist, significantly inhibited the induced release of t-PA and vWF, while the 'intracellular calcium antagonist' TMB-8 had no effect. Lanthanum chloride (200 μM) inhibited the induced release of t-PA but not that of vWF. Our results suggest that Ca2+ influx is essential for the release of t-PA and vWF from the perfused rat hindleg.
Topics
TNO Identifier
231379
ISSN
03406245
Source
Thrombosis and Haemostasis, 66(4), pp. 479-483.
Pages
479-483
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