PAR-1 thrombin receptor antagonist

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Effects of thrombin, PAR-1 activating peptide and a PAR-1 antagonist on umbilical artery resistance in vitro

BACKGROUND The non-thrombotic effects of thrombin in cardiovascular tissues, as mediated via the protease activated receptors (PARs), and particularly PAR-1, have been the focus of much recent research. The aims of this study were to evaluate the effects of thrombin, a specific PAR-1 activating peptide (PAR1-AP), and a PAR-1 antagonist on human umbilical artery tone in vitro. METHODS Human um...

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Cardiovascular responses mediated by protease-activated receptor-2 (PAR-2) and thrombin receptor (PAR-1) are distinguished in mice deficient in PAR-2 or PAR-1.

We developed mice deficient in protease-activated receptor-2 (PAR-2) or PAR-1 to explore the pathophysiological functions of these receptors. In this report, we evaluated mean arterial pressure and heart rate (HR) changes in response to PAR-1 or PAR-2 activation in anesthetized wild-type (WT), PAR-1-deficient (PAR-1(-/-)), and PAR-2-deficient (PAR-2(-/-)) mice. In WT mice, TFLLRNPNDK, a PAR-1 s...

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Receptor binding and agonist efficacy: new insights from mutants of the thrombin protease-activated receptor-1 (PAR-1).

The article by Blackhart et al. (2000), describing the differential activation of mutated thrombin protease-activated receptor-1 (PAR-1) either by the proteolytically revealed tethered ligand or by soluble receptor-activating peptides, adds yet another challenge to the theoretical understanding of receptor mechanisms. It is useful to view these new findings with the perspective offered by class...

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Protein kinase Cβ regulates heterologous desensitization of thrombin receptor (PAR-1) in endothelial cells.

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Time course of recovery of endothelial cell surface thrombin receptor (PAR-1) expression.

We studied dynamics of cell surface expression of proteolytically activated thrombin receptor (PAR-1) in human pulmonary artery endothelial cells (HPAEC). PAR-1 activation was measured by changes in cytosolic calcium concentration ([Ca2+]i) and HPAEC retraction response (determined by real-time transendothelial monolayer electrical resistance). [Ca2+]iincrease in response to thrombin was abolis...

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ژورنال

عنوان ژورنال: Japanese Journal of Thrombosis and Hemostasis

سال: 2012

ISSN: 1880-8808,0915-7441

DOI: 10.2491/jjsth.23.47