AJP - Regu Ad Instruments
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
 QUICK SEARCH:   [advanced]


     


Am J Physiol Regul Integr Comp Physiol 291: R719-R727, 2006. First published April 6, 2006; doi:10.1152/ajpregu.00825.2005
0363-6119/06 $8.00
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow All Versions of this Article:
291/3/R719    most recent
00825.2005v1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in Web of Science
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 Web of Science (1)
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Rowe, K. D.
Right arrow Articles by Knuepfer, M. M.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Rowe, K. D.
Right arrow Articles by Knuepfer, M. M.

NEUROHUMORAL CONTROL OF CARDIOVASCULAR FUNCTION

Central angiotensin II receptors mediate hemodynamic response variability to stressors

Kayla D. Rowe, Julie A. Schwartz, Lance L. Lomax, and Mark M. Knuepfer

Department of Pharmacological and Physiological Science, St Louis University School of Medicine, St. Louis, Missouri

Submitted 23 November 2005 ; accepted in final form 18 March 2006

We examined whether ANG II receptors in the central nervous system mediate hemodynamic responses to pharmacological (cocaine) and behavioral (cold water) stressors. After administration of cocaine (5 mg/kg iv), rats were classified as vascular responders (VR) if their pressor response was due entirely to an increase in systemic vascular resistance (SVR) despite a decrease in cardiac output (CO). Cocaine elicited a pressor response in mixed responders (MR) that was dependent on small increases in both SVR and CO. ANG II (30 ng/5 µl icv, 5 min before cocaine) augmented the decrease in CO in VR and prevented the increase in CO in MR. Administration of [Sar1,Thr8]ANG II (20 µg/5 µl icv; sarthran) before cocaine attenuated the decrease in CO and the large increase in SVR in VR so that they were no longer different from MR. Losartan (20 µg icv) or captopril (50 µg icv) preceding cocaine administration also attenuated the decrease in CO and the large increase in SVR seen in VR only. The role of angiotensin was not specific for cocaine, because ANG II (icv) pretreatment before startle with cold water (1 cm deep) enhanced the decrease in CO and the increase in SVR in both MR and VR, whereas losartan (icv) pretreatment before startle attenuated the decrease in CO and the increase in SVR in VR so that they were no longer different from MR. These data suggest that central ANG II receptors mediate the greater vascular and cardiac responsiveness in vascular responders to acute pharmacological and behavioral stressors.

renin-angiotensin system; cardiac output; systemic vascular resistance; startle; cocaine; central nervous system



Address for reprint requests and other correspondence: M. M. Knuepfer, Dept. of Pharmacological and Physiological Science, St. Louis Univ. School of Medicine, 1402 S. Grand Blvd., St. Louis, MO 63104 (e-mail: knuepfmm{at}slu.edu)




This article has been cited by other articles:


Home page
Am. J. Physiol. Regul. Integr. Comp. Physiol.Home page
J. A. Schwartz, N. S. Reilly, and M. M. Knuepfer
Angiotensin and NMDA receptors in the median preoptic nucleus mediate hemodynamic response patterns to stress
Am J Physiol Regulatory Integrative Comp Physiol, July 1, 2008; 295(1): R155 - R165.
[Abstract] [Full Text] [PDF]




HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Visit Other APS Journals Online
Copyright © 2006 by the American Physiological Society.