J Physiol Society Meetings
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
 QUICK SEARCH:   [advanced]


     


J Physiol Volume 574, Number 2, 597-604, July 15, 2006 DOI: 10.1113/jphysiol.2006.107326
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow All Versions of this Article:
574/2/597    most recent
jphysiol.2006.107326v1
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Huang, C.
Right arrow Articles by Johns, E. J.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Huang, C.
Right arrow Articles by Johns, E. J.
Related Collections
Right arrow Integrative

INTEGRATIVE

The contribution of brain angiotensin II to the baroreflex regulation of renal sympathetic nerve activity in conscious normotensive and hypertensive rats

Chunlong Huang1, Misa Yoshimoto2, Kenju Miki2 and Edward J. Johns1

1 Department of Physiology, University College Cork, Cork, Ireland
2 Department of Environmental Health, Life Science and Human Technology, Nara Women's University, Nara, Japan

Angiotensin II receptor density in the brain is elevated when dietary salt intake is raised or in the state of hypertension. The aim of this study was to evaluate whether the angiotensin II modulation of the baroreceptor control of renal sympathetic nerve activity was altered under these conditions. Wistar rats, fed either a regular (0.25% w/w sodium) or high-salt diet (3.1% w/w sodium), or stroke-prone spontaneously hypertensive rats (SHRSPs) were implanted with cannulae in the carotid artery, jugular vein and the cerebroventricle and with recording electrodes on the renal sympathetic nerves. Three days later, baroreceptor gain curves were generated for renal sympathetic nerve activity and heart rate before and following intracerebroventricular (I.C.V.) administration of losartan (15 µg) to block angiotensin AT1 receptors. The rats fed a regular diet had a mean blood pressure of 116 ± 3 mmHg and heart rate of 467 ± 25 beats min–1, which remained unchanged after the I.C.V. administration of losartan. The sensitivity or curvature coefficient of the baroreceptor curve for renal sympathetic nerve activity was increased by 36% (P < 0.05) following losartan. In the rats fed a high-salt diet, all cardiovascular variables and the losartan-induced increase in the baroreceptor curvature coefficient for renal sympathetic nerve activity (29%) were similar to values in rats on the regular sodium diet. The heart rate baroreceptor curvature coefficient was not altered in either the rats fed a regular or a high-salt diet. The slope of the renal sympathetic nerve activity baroreflex gain curve in the SHRSPs was less and the increase following administration of losartan (54%) was greater than in the Wistar rats. These data indicate that in the conscious state, the tonic inhibitory action of brain angiotensin II on the baroreflex regulation of renal sympathetic nerve activity was unaffected by raised dietary sodium, but its role was enhanced in the SHRSPs.

(Received 21 February 2006; accepted after revision 6 May 2006; first published online 11 May 2006)
Corresponding author E. J. Johns: Department of Physiology, Aras Windle, University College Cork, Cork, Republic of Ireland. Email: e.j.johns{at}ucc.i.e




This article has been cited by other articles:


Home page
Exp PhysiolHome page
E. T. Flanagan, M. M. Buckley, C. M. Aherne, F. Lainis, M. Sattar, and E. J. Johns
Impact of cardiac hypertrophy on arterial and cardiopulmonary baroreflex control of renal sympathetic nerve activity in anaesthetized rats
Exp Physiol, September 1, 2008; 93(9): 1058 - 1064.
[Abstract] [Full Text] [PDF]




HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Copyright © 2006 The Physiological Society.