Amplification of the COX/TXS/TP receptor pathway enhances uridine diphosphate-induced contraction by advanced glycation end products in rat carotid arteries.
Animals
Carotid Arteries
/ drug effects
Endothelium, Vascular
/ drug effects
Glycation End Products, Advanced
/ metabolism
Male
Muscle, Smooth, Vascular
/ drug effects
Nitric Oxide Synthase
/ metabolism
Prostaglandin-Endoperoxide Synthases
/ metabolism
Rats
Rats, Wistar
Receptors, Thromboxane
/ metabolism
Signal Transduction
/ drug effects
Thromboxane-A Synthase
/ metabolism
Uridine Diphosphate
/ pharmacology
Vasoconstriction
/ drug effects
Advanced glycation end products
Carotid arteries
Contraction
Thromboxane-prostanoid receptor
Uridine diphosphate
Vascular smooth muscle
Journal
Pflugers Archiv : European journal of physiology
ISSN: 1432-2013
Titre abrégé: Pflugers Arch
Pays: Germany
ID NLM: 0154720
Informations de publication
Date de publication:
12 2019
12 2019
Historique:
received:
24
08
2019
accepted:
08
11
2019
revised:
07
11
2019
pubmed:
19
11
2019
medline:
15
5
2020
entrez:
19
11
2019
Statut:
ppublish
Résumé
Advanced glycation end products (AGEs) play a pivotal role in vascular functions under various pathophysiological conditions. Although uridine diphosphate (UDP) is an important extracellular nucleotide, the relationship between AGEs and UDP regarding their effect on vascular functions remains unclear. Therefore, we investigated the effects of AGE-bovine serum albumin (AGE-BSA) on UDP-mediated responses in rat thoracic aorta and carotid arteries. In rat thoracic aorta, UDP-induced relaxation was observed and this relaxation was similar between control (1.0 v/v% PBS) and AGE-BSA-treated (0.1 mg/mL for 60 min) groups. In contrast, contraction but not relaxation was obtained following UDP application to carotid arteries with and without endothelia; contraction was greater in the AGE-BSA-treated group than in the control group. The difference in UDP-induced contraction between the two groups was not abolished by the use of a nitric oxide synthase (NOS) inhibitor, whereas it was abolished by the use of cyclooxygenase (COX), thromboxane synthase (TXS), and thromboxane-prostanoid (TP) receptor antagonist. Further, the difference in UDP-induced contraction was not abolished by the use of a cPLA
Identifiants
pubmed: 31736003
doi: 10.1007/s00424-019-02330-y
pii: 10.1007/s00424-019-02330-y
doi:
Substances chimiques
Glycation End Products, Advanced
0
Receptors, Thromboxane
0
Uridine Diphosphate
58-98-0
Nitric Oxide Synthase
EC 1.14.13.39
Prostaglandin-Endoperoxide Synthases
EC 1.14.99.1
Thromboxane-A Synthase
EC 5.3.99.5
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
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