ArticleBritish journal of pharmacology2002
Enzymatic activation of endothelial protease-activated receptors is dependent on artery diameter in human and porcine isolated coronary arteries.
Article in British journal of pharmacology, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
4 citing papers in PubMed, 26 citations in OpenAlex.
- Modulation of PAR(1) signalling by benzimidazole compounds.British journal of pharmacology · 2012Article
- Quercetin and its major metabolites selectively modulate cyclic GMP-dependent relaxations and associated tolerance in pig isolated coronary artery.British journal of pharmacology · 2010Article
- Proteinases and signalling: pathophysiological and therapeutic implications via PARs and more.British journal of pharmacology · 2008Review
- The contribution of protease-activated receptor 1 to neuronal damage caused by transient focal cerebral ischemia.Proceedings of the National Academy of Sciences of the United States of America · 2003Article
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Protease-activated receptor (PAR)-mediated vascular relaxations have been compared in coronary arteries of different diameters isolated from both humans and pigs. Thrombin, trypsin, and the PAR1-activating peptide, TFLLR, all caused concentration-dependent relaxation of both large (epicardial; approximately 2 mm internal diameter) and small (intramyocardial; approximately 200 microm internal diameter) human coronary arteries. EC(50) values for thrombin (0.006 u ml(-1) in epicardial, 1.69 u ml(-1) in intramyocardial) and trypsin (0.02 u ml(-1) in epicardial, 1.05 u ml(-1) in intramyocardial) were significantly (P<0.01) greater in intramyocardial arteries. By contrast, EC(50) values for TFLLR were not different between epicardial (0.35 microM) and intramyocardial (0.43 microM) arteries. In porcine coronary arteries, EC(50) values for relaxations to thrombin (0.03 u ml(-1) in epicardial 0.17 u ml(-1) in intramyocardial) were also significantly (P<0.01) greater in the smaller arteries. EC(50) values for both TFLLR and the PAR2-activating peptide, SLIGKV, were not different between the two different-sized pig coronary arteries. PAR1-immunoreactivity was localized to the endothelium of human epicardial and intramyocardial arteries and both PAR1- and PAR2-immunoreactivity was observed in endothelial cells of equivalent porcine arteries. These findings indicate that enzymatic activation of endothelial cell PARs in human (PAR1) and porcine (PAR1 and PAR2) coronary arteries is markedly reduced in intramyocardial arteries when compared with epicardial arteries, suggesting increased regulation of PAR-mediated vascular responses in resistance-type arteries.
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