Show simple item record

dc.contributor.authorBodkin, JVen_US
dc.contributor.authorThakore, Pen_US
dc.contributor.authorAubdool, AAen_US
dc.contributor.authorLiang, Len_US
dc.contributor.authorFernandes, ESen_US
dc.contributor.authorNandi, Men_US
dc.contributor.authorSpina, Den_US
dc.contributor.authorClark, JEen_US
dc.contributor.authorAaronson, PIen_US
dc.contributor.authorShattock, MJen_US
dc.contributor.authorBrain, SDen_US
dc.date.accessioned2016-09-13T13:59:44Z
dc.date.available2014-04-24en_US
dc.date.issued2014-08en_US
dc.date.submitted2016-08-23T15:04:52.294Z
dc.identifier.issn2052-1707en_US
dc.identifier.urihttp://qmro.qmul.ac.uk/xmlui/handle/123456789/15222
dc.description.abstractRadiotelemetry was used to investigate the in vivo cardiovascular and activity phenotype of both TRPA1 (transient receptor potential ankyrin 1) wild-type (WT) and TRPA1 knockout (KO) mice. After baseline recording, experimental hypertension was induced using angiotensin II infusion (1.1 mg(-1) kg(-1) a day, for 14 days). TRPA1 WT and KO mice showed similar morphological and functional cardiovascular parameters, including similar basal blood pressure (BP), heart rate, size, and function. Similar hypertension was also displayed in response to angiotensin II (156 ± 7 and 165 ± 11 mmHg, systolic BP ± SEM, n = 5-6). TRPA1 KO mice showed increased hypertensive hypertrophy (heart weight:tibia length: 7.3 ± 1.6 mg mm(-1) vs. 8.8 ± 1.7 mg mm(-1)) and presented with blunted interleukin 6 (IL-6) production compared with hypertensive WT mice (151 ± 24 vs. 89 ± 16 pg mL(-1)). TRPA1 expression in dorsal root ganglion (DRG) neurones was upregulated during hypertension (163% of baseline expression). Investigations utilizing the TRPA1 agonist cinnamaldehyde (CA) on mesenteric arterioles isolated from näive mice suggested a lack of TRPA1-dependent vasoreactivity in this vascular bed; a site with notable ability to alter total peripheral resistance. However, mesenteric arterioles isolated from TRPA1 KO hypertensive mice displayed significantly reduced ability to relax in response to nitric oxide (NO) (P < 0.05). Unexpectedly, naïve TRPA1 KO mice also displayed physical hyperactivity traits at baseline, which was exacerbated during hypertension. In conclusion, our study provides a novel cardiovascular characterization of TRPA1 KO mice in a model of hypertension. Results suggest that TRPA1 has a limited role in global cardiovascular control, but we demonstrate an unexpected capacity for TRPA1 to regulate physical activity.en_US
dc.format.extente00052 - ?en_US
dc.languageengen_US
dc.language.isoenen_US
dc.relation.ispartofPharmacol Res Perspecten_US
dc.rightsCC-BY
dc.subjectBlood pressureen_US
dc.subjectTRPA1en_US
dc.subjectcinnamaldehydeen_US
dc.subjecthypertensionen_US
dc.subjectlocomotionen_US
dc.titleInvestigating the potential role of TRPA1 in locomotion and cardiovascular control during hypertension.en_US
dc.typeArticle
dc.rights.holder© 2014 The Authors.
dc.identifier.doi10.1002/prp2.52en_US
pubs.author-urlhttps://www.ncbi.nlm.nih.gov/pubmed/25505598en_US
pubs.issue4en_US
pubs.notesNot knownen_US
pubs.publication-statusPublisheden_US
pubs.volume2en_US
dcterms.dateAccepted2014-04-24en_US


Files in this item

Thumbnail

This item appears in the following Collection(s)

Show simple item record