dc.contributor.author |
Guild, SJ |
en |
dc.contributor.author |
McBryde, FD |
en |
dc.contributor.author |
Malpas, SC |
en |
dc.contributor.author |
Barrett, CJ |
en |
dc.coverage.spatial |
United States |
en |
dc.date.accessioned |
2014-01-13T02:34:58Z |
en |
dc.date.available |
2014-01-13T02:34:58Z |
en |
dc.date.issued |
2012 |
en |
dc.identifier.citation |
Hypertension 59(3):614-620 Mar 2012 |
en |
dc.identifier.other |
1524-4563 |
en |
dc.identifier.other |
HYPERTENSIONAHA.111.180885 |
en |
dc.identifier.uri |
http://hdl.handle.net/2292/21387 |
en |
dc.description.abstract |
Overactivity of the sympathetic nervous system has long been implicated in the hypertensive response to elevated angiotensin II (Ang II) levels. Although recent studies suggest that high dietary salt may alter cardiovascular responses to Ang II, direct evidence demonstrating chronic activation of sympathetic nerve activity is lacking. The objective of this study was to determine whether a low dose of Ang II, on a background of high salt intake, would result in a chronic increase in renal sympathetic nerve activity (RSNA). Arterial pressure and RSNA were recorded via telemetry. Two groups of rabbits were studied: 1 group drank a 0.9% NaCl solution and received Ang II (20 ng/kg per minute for 21 days, Salt+Ang), and the other drank tap water throughout and was not infused with Ang II (Control). In the Salt+Ang group, mean arterial pressure increased over the first week and remain elevated by 18.5±4.1 mm Hg at day 21. RSNA was not significantly different between groups on day 7 but was significantly elevated in the Salt+Ang group on day 21 (13.5±3.2% compared with 6.8±0.8% in the Control group; P<0.05). Baroreflex control of RSNA showed a rightward shift on day 21, but not day 7, and baroreflex responses indicated that RSNA could not be completely suppressed when arterial pressure was increased. No changes were observed in either mean arterial pressure or RSNA variables in the Control group. Our results support the hypothesis that elevated Ang II levels, in conjunction with a high salt diet, have the ability to chronically increase RSNA and, thus, potentially contribute to the maintenance of hypertension. |
en |
dc.language |
eng |
en |
dc.relation.ispartofseries |
Hypertension |
en |
dc.rights |
Items in ResearchSpace are protected by copyright, with all rights reserved, unless otherwise indicated. Previously published items are made available in accordance with the copyright policy of the publisher. Details obtained from http://atvb.ahajournals.org/site/misc/ifora.xhtml#copyright http://www.sherpa.ac.uk/romeo/issn/0194-911X/ |
en |
dc.rights.uri |
https://researchspace.auckland.ac.nz/docs/uoa-docs/rights.htm |
en |
dc.subject |
Action Potentials |
en |
dc.subject |
Angiotensin II |
en |
dc.subject |
Animals |
en |
dc.subject |
Baroreflex |
en |
dc.subject |
Blood Pressure |
en |
dc.subject |
Chronic Disease |
en |
dc.subject |
Disease Models, Animal |
en |
dc.subject |
Female |
en |
dc.subject |
Follow-Up Studies |
en |
dc.subject |
Hypertension |
en |
dc.subject |
Kidney |
en |
dc.subject |
Male |
en |
dc.subject |
Rabbits |
en |
dc.subject |
Sodium Chloride, Dietary |
en |
dc.subject |
Sympathetic Nervous System |
en |
dc.subject |
Telemetry |
en |
dc.title |
High dietary salt and angiotensin II chronically increase renal sympathetic nerve activity: a direct telemetric study. |
en |
dc.type |
Journal Article |
en |
dc.identifier.doi |
10.1161/HYPERTENSIONAHA.111.180885 |
en |
pubs.issue |
3 |
en |
pubs.begin-page |
614 |
en |
pubs.volume |
59 |
en |
pubs.author-url |
http://www.ncbi.nlm.nih.gov/pubmed/22275533 |
en |
pubs.end-page |
620 |
en |
dc.rights.accessrights |
http://purl.org/eprint/accessRights/RestrictedAccess |
en |
pubs.elements-id |
286082 |
en |
pubs.org-id |
Bioengineering Institute |
en |
pubs.org-id |
ABI Associates |
en |
pubs.org-id |
Faculty of Medical & Hlth Sci |
en |
pubs.org-id |
Medical Sciences |
en |
pubs.org-id |
Physiology Division |
en |