AJP - Regu Track the topics, authors and articles important to you
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
 QUICK SEARCH:   [advanced]


     


Am J Physiol Regul Integr Comp Physiol 297: R330-R336, 2009. First published May 27, 2009; doi:10.1152/ajpregu.90867.2008
0363-6119/09 $8.00
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Supplemental Figures
Right arrow All Versions of this Article:
297/2/R330    most recent
90867.2008v1
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 Web of Science (2)
Google Scholar
Right arrow Articles by Yosten, G. L. C.
Right arrow Articles by Samson, W. K.
PubMed
Right arrow PubMed Citation
Right arrow Articles by Yosten, G. L. C.
Right arrow Articles by Samson, W. K.

ARTICLES

Nesfatin-1 exerts cardiovascular actions in brain: possible interaction with the central melanocortin system

Gina L. C. Yosten and Willis K. Samson

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

Submitted 27 October 2008 ; accepted in final form 20 May 2009

Nesfatin-1 is a recently discovered hypothalamic peptide that was shown to suppress food intake through a melanocortin-3/4 receptor-dependent mechanism. Since nesfatin-1 mRNA is detected in the paraventricular nucleus of the hypothalamus, and because many peptides that alter food intake also influence cardiovascular function, we tested the ability of centrally administered nesfatin-1 to affect mean arterial pressure (MAP) in conscious, freely moving rats. Significant increases in MAP were observed following intracerebroventricular administration of nesfatin-1. Pretreatment with either the melanocortin-3/4 receptor antagonist, SHU9119 (intracerebroventricular), or the {alpha}-adrenergic antagonist, phentolamine (intra-arterial), abrogated the rise in MAP induced by nesfatin-1, indicating that nesfatin-1 may interact with the central melanocortin system to increase sympathetic nerve activity and lead to an increase in MAP. Thus we have identified a novel action of nesfatin-1, in addition to its anorexigenic effects, to stimulate autonomic nervous system activity.

autonomics; hypothalamus; appetite



Address for reprint requests and other correspondence: G. L. C. Yosten, Saint Louis Univ., Dept. of Pharmacological and Physiological Science, 1402 S. Grand Blvd., St. Louis, MO 63104 (e-mail: gyosten{at}slu.edu)







HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Visit Other APS Journals Online
Copyright © 2009 by the American Physiological Society.