Changes in aortic reactivity associated with the loss of equilibrative nucleoside transporter 1 (ENT1) in mice

Slc29a1 encodes for equilibrative nucleoside transporter subtype 1 (ENT1), the primary mechanism of adenosine transfer across cell membranes. Previous studies showed that tissues isolated from Slc29a1-null mice are relatively resistant to injury caused by vascular ischemia-reperfusion. To determine...

Full description

Saved in:
Bibliographic Details
Published in:PloS one 2018-11, Vol.13 (11), p.e0207198-e0207198
Main Authors: Best, K Arielle, Bone, Derek B, Vilas, Gonzalo, Gros, Robert, Hammond, James R
Format: Article
Language:English
Subjects:
Adenosine
Adenosine - blood
Adenosine - pharmacology
Animals
Aorta
Aorta, Thoracic - drug effects
Aorta, Thoracic - pathology
Aorta, Thoracic - physiopathology
Arteries
Biology and Life Sciences
Blood pressure
Cell membranes
Contractility
Coronary vessels
Endothelium
Equilibrative Nucleoside Transporter 1 - antagonists & inhibitors
Equilibrative Nucleoside Transporter 1 - genetics
Equilibrative Nucleoside Transporter 1 - physiology
Gene Expression
Hemodynamics
Hypoxia
Hypoxia - genetics
Hypoxia - pathology
Hypoxia - physiopathology
In Vitro Techniques
In vivo methods and tests
Ischemia
Kinases
Laboratory animals
Macrostructure
Male
Medicine and Health Sciences
Membranes
Mice
Mice, Inbred C57BL
Mice, Knockout
Microvasculature
Mineralization
Nucleoside transporter
Nucleosides
Pharmacology
Phenylephrine
Physiology
Potassium chloride
Reperfusion
Rodents
Thorax
Tissues
Vasoconstriction - drug effects
Vasoconstriction - genetics
Vasoconstriction - physiology
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:Slc29a1 encodes for equilibrative nucleoside transporter subtype 1 (ENT1), the primary mechanism of adenosine transfer across cell membranes. Previous studies showed that tissues isolated from Slc29a1-null mice are relatively resistant to injury caused by vascular ischemia-reperfusion. To determine if there are similar changes in the microvasculature, and investigate underlying mechanism, we examined aortas isolated from wildtype and Slc29a1-null mice. Aorta macrostructure and gene expression were examined histologically and by qPCR, respectively. Wire myography was used to assess the contractile properties of isolated thoracic aortic rings and their response to adenosine under both normoxic and hypoxic conditions. In vivo haemodynamic parameters were assessed using the tail-cuff method. Slc29a1-null mice had significantly (P
ISSN:1932-6203
1932-6203
DOI:10.1371/journal.pone.0207198