dc.contributor.author | Ho, Ming-Fen | |
dc.contributor.author | Low, Leanne M | |
dc.contributor.author | Rose'Meyer, Roselyn B | |
dc.date.accessioned | 2018-01-19T05:55:54Z | |
dc.date.available | 2018-01-19T05:55:54Z | |
dc.date.issued | 2016 | |
dc.identifier.issn | 1932-6203 | |
dc.identifier.doi | 10.1371/journal.pone.0150021 | |
dc.identifier.uri | http://hdl.handle.net/10072/100586 | |
dc.description.abstract | Background
Essential hypertension is considered to be a multifactorial disorder and its aetiology has yet
to be clearly identified. As the adenosine receptors have a significant role in mediating vasodilation,
alterations in their structures or signalling pathways may be involved in the development
of hypertension. This study aimed to measure the expression of adenosine A3
receptors in a range of cardiovascular tissues and determine whether they could be altered
with essential hypertension, and to functionally test responses to adenosine A3 receptor
agonists in coronary blood vessels using the isolated perfused heart preparation.
Methods
mRNA samples from cardiovascular tissues and a range of blood vessels were collected
from 10 week old male spontaneously hypertensive rats and age-gender matched Wistar
rats (n = 8). The Langendorff heart perfusion preparation was used to characterise adenosine
A3 receptor mediated coronary vasodilation in the rat heart.
Results
Adenosine A3 receptor agonists induced coronary vasodilation. The expression of adenosine
A3 receptors in cardiovascular tissues was altered in a tissue-specific pattern. Specifically,
down-regulation of adenosine A3 receptor expression occurred in hypertensive
hearts, which might be associated with attenuated vasodilator responses observed in coronary
vessels to adenosine A3 receptor agonists.
Conclusions
This study demonstrated alterations in the expression of adenosine A3 receptors occurred in a
tissue specific mode, and reduced adenosine A3 receptor mediated coronary vasodilation in
hearts from spontaneously hypertensive rats. Our findings with regard to changes in the adenosine
A3 receptor in hypertensive hearts suggest that adenosine A3 receptor might play a role in
the physiopathology of essential hypertension and potentially open the way to pharmacologic
manipulation of vasomotor activity by the use of adenosine A3 receptor agonists. | |
dc.description.peerreviewed | Yes | |
dc.language | English | |
dc.language.iso | eng | |
dc.publisher | Public Library of Sciences | |
dc.relation.ispartofpagefrom | e0150021-1 | |
dc.relation.ispartofpageto | e0150021-15 | |
dc.relation.ispartofissue | 2 | |
dc.relation.ispartofjournal | PLoS One | |
dc.relation.ispartofvolume | 11 | |
dc.subject.fieldofresearch | Clinical pharmacology and therapeutics | |
dc.subject.fieldofresearchcode | 321402 | |
dc.title | Pharmacology of the Adenosine A3 Receptor in the Vasculature and Essential Hypertension | |
dc.type | Journal article | |
dc.type.description | C1 - Articles | |
dc.type.code | C - Journal Articles | |
dcterms.license | https://creativecommons.org/licenses/by/4.0/ | |
dc.description.version | Version of Record (VoR) | |
gro.faculty | Griffith Health, School of Medical Science | |
gro.rights.copyright | © 2016 Ho et al. This is an open access
article distributed under the terms of the Creative
Commons Attribution License, which permits
unrestricted use, distribution, and reproduction in any
medium, provided the original author and source are
credited. | |
gro.hasfulltext | Full Text | |
gro.griffith.author | Rose'Meyer, Roselyn B. | |