Vascular effects of proteinase-activated receptor 2 agonist peptide
(1997) In Journal of Vascular Research 34(4). p.267-272- Abstract
- Proteinase-activated receptor 2 (PAR-2) is a G protein-coupled receptor related to the thrombin receptor. PAR-2 can be activated by trypsin and by synthetic peptides corresponding to the new amino terminus generated by activating proteolytic cleavage. We show in this report that intravenous injection of PAR-2 agonist peptides has dramatic effects on arterial blood pressure in anesthetized rats. The peptide SLIGRLETQPPI, at 150 nmol/kg, transiently decreased the mean arterial pressure from 104 to 60 mm Hg. The hypotensive response was dose-dependent, and was not secondary to effects on central vasoregulatory systems, heart rate, or the kidneys. A nitric oxide synthase inhibitor attenuated the hypotensive response induced by the PAR-2... (More)
- Proteinase-activated receptor 2 (PAR-2) is a G protein-coupled receptor related to the thrombin receptor. PAR-2 can be activated by trypsin and by synthetic peptides corresponding to the new amino terminus generated by activating proteolytic cleavage. We show in this report that intravenous injection of PAR-2 agonist peptides has dramatic effects on arterial blood pressure in anesthetized rats. The peptide SLIGRLETQPPI, at 150 nmol/kg, transiently decreased the mean arterial pressure from 104 to 60 mm Hg. The hypotensive response was dose-dependent, and was not secondary to effects on central vasoregulatory systems, heart rate, or the kidneys. A nitric oxide synthase inhibitor attenuated the hypotensive response induced by the PAR-2 agonist peptide. Further experiments in vitro, on preparations of rat femoral artery and vein, showed that PAR-2 agonist peptide elicited a dose-dependent relaxation of both types of vessel. Removal of the endothelium abolished the agonist peptide-induced relaxation. Our results demonstrate that activation of PAR-2 can modulate vascular tone, and that this response was an effect mediated at least partly by nitric oxide. The effect on blood vessels further suggests that the physiological activator of this proteolytically activated receptor is an enzyme present and active in the blood, possibly after a vascular injury. (Less)
Please use this url to cite or link to this publication:
https://lup.lub.lu.se/record/1112060
- author
- Emilsson, K ; Wahlestedt, C ; Sun, M K ; Nystedt, Sverker LU ; Owman, Christer LU and Sundelin, Johan LU
- organization
- publishing date
- 1997
- type
- Contribution to journal
- publication status
- published
- subject
- in
- Journal of Vascular Research
- volume
- 34
- issue
- 4
- pages
- 267 - 272
- publisher
- Karger
- external identifiers
-
- pmid:9256086
- scopus:0030879202
- ISSN
- 1423-0135
- language
- English
- LU publication?
- yes
- id
- 5bc0ae06-fdb6-4e93-8a91-cd79f2dcf7bd (old id 1112060)
- date added to LUP
- 2016-04-01 15:51:09
- date last changed
- 2022-01-28 07:33:16
@article{5bc0ae06-fdb6-4e93-8a91-cd79f2dcf7bd,
abstract = {{Proteinase-activated receptor 2 (PAR-2) is a G protein-coupled receptor related to the thrombin receptor. PAR-2 can be activated by trypsin and by synthetic peptides corresponding to the new amino terminus generated by activating proteolytic cleavage. We show in this report that intravenous injection of PAR-2 agonist peptides has dramatic effects on arterial blood pressure in anesthetized rats. The peptide SLIGRLETQPPI, at 150 nmol/kg, transiently decreased the mean arterial pressure from 104 to 60 mm Hg. The hypotensive response was dose-dependent, and was not secondary to effects on central vasoregulatory systems, heart rate, or the kidneys. A nitric oxide synthase inhibitor attenuated the hypotensive response induced by the PAR-2 agonist peptide. Further experiments in vitro, on preparations of rat femoral artery and vein, showed that PAR-2 agonist peptide elicited a dose-dependent relaxation of both types of vessel. Removal of the endothelium abolished the agonist peptide-induced relaxation. Our results demonstrate that activation of PAR-2 can modulate vascular tone, and that this response was an effect mediated at least partly by nitric oxide. The effect on blood vessels further suggests that the physiological activator of this proteolytically activated receptor is an enzyme present and active in the blood, possibly after a vascular injury.}},
author = {{Emilsson, K and Wahlestedt, C and Sun, M K and Nystedt, Sverker and Owman, Christer and Sundelin, Johan}},
issn = {{1423-0135}},
language = {{eng}},
number = {{4}},
pages = {{267--272}},
publisher = {{Karger}},
series = {{Journal of Vascular Research}},
title = {{Vascular effects of proteinase-activated receptor 2 agonist peptide}},
volume = {{34}},
year = {{1997}},
}