Skip Navigation

Cardiovascular Research 2001 50(1):137-144; doi:10.1016/S0008-6363(01)00193-6
© 2001 by European Society of Cardiology
This Article
Right arrow Full Text Freely available
Right arrow FREE Full Text (PDF) Freely available
Right arrow E-letters: Submit a response
Right arrow Alert me when this article is cited
Right arrow Alert me when E-letters are posted
Right arrow Alert me if a correction is posted
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 Add to My Personal Archive
Right arrow Download to citation manager
Right arrowRequest Permissions
Right arrow Disclaimer
Google Scholar
Right arrow Articles by Sullivan, J. C.
Right arrow Articles by Davison, C. A.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Sullivan, J. C.
Right arrow Articles by Davison, C. A.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

Copyright © 2001, European Society of Cardiology

Effect of age on electrical field stimulation (EFS)-induced endothelium-dependent vasodilation in male and female rats

Jennifer C. Sullivan* and Cathy A. Davison

Center for Cardiovascular Sciences, Albany Medical College, Albany, NY, USA

* Corresponding author. Medical College of Georgia, 1459 Laney-Walker Blvd. CB 3213, Augusta, GA 30912, USA. Tel.: +1-706-721-6164; fax: +1-706-721-9799 jsullivan{at}mail.mcg.edu

Objective: The purpose of this study was to determine whether the effect of age on electrical field stimulation (EFS)-induced endothelium-dependent vasodilation was different in males and females. Methods: Young (3 month) and old (25 month) Fisher 344 rats were studied: young females (YF, n = 34), young males (YM, n = 28), old females (OF, n = 19), and old males (OM, n = 24). Isolated mesenteric resistance arteries (endothelium-intact and denuded) were pressurized, and outer diameter was monitored. EFS-response curves (0.1–8 Hz) were performed in preconstricted arteries in the presence of guanethidine. EFS responses were expressed as percent relaxation from preconstricted diameter. Area under the curve (AUC) was calculated and comparisons were made using ANOVA and t-tests. Results: Males became less responsive to EFS-induced vasodilation with age, while responses among females were unaffected (AUC: YM=344±23, OM=253±25, P = 0.008; YF=397±21, OF=365±25, P = 0.33). Endothelial denudation produced a significant decrease in EFS-induced dilation among all rat groups. The effect of denudation was greater in young animals compared to old. Incubation with the nitric oxide synthase inhibitor N{omega}-nitro-L-arginine (LNA) significantly decreased EFS responsiveness among all of the rat groups. Conclusions: EFS-induced vasodilation declines with age among males. In YF and YM endothelium-dependent EFS-induced vasodilation is mediated by the release of endothelium-derived NO. With age, endothelial function declines, which is likely due to a decrease in the production of endothelium-derived NO. A decline in endothelial-derived NO is likely responsible for the decrease in EFS-induced vasodilation with age among males.

KEYWORDS EFS, electrical field stimulation; YF, young female; OF, old female; YM, young male; OM, old male; LNA, N{omega}-nitro-L-arginine; TTX, tetrodotoxin; NO, nitric oxide


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?


This article has been cited by other articles:


Home page
 Am. J. Physiol. Heart Circ. Physiol.Home page
X. F. Figueroa, C.-C. Chen, K. P. Campbell, D. N. Damon, K. H. Day, S. Ramos, and B. R. Duling
Are voltage-dependent ion channels involved in the endothelial cell control of vasomotor tone?
Am J Physiol Heart Circ Physiol, September 1, 2007; 293(3): H1371 - H1383.
[Abstract] [Full Text] [PDF]

Home page
 EndocrinologyHome page
G. R. Ross, M. Chauhan, P. R. Gangula, L. Reed, C. Thota, and C. Yallampalli
Female Sex Steroids Increase Adrenomedullin-Induced Vasodilation by Increasing the Expression of Adrenomedullin2 Receptor Components in Rat Mesenteric Artery
Endocrinology, January 1, 2006; 147(1): 389 - 396.
[Abstract] [Full Text] [PDF]

Home page
 J. Appl. Physiol.Home page
J. C. Sullivan, E. D. Loomis, M. Collins, J. D. Imig, E. W. Inscho, and J. S. Pollock
Age-related alterations in NOS and oxidative stress in mesenteric arteries from male and female rats
J Appl Physiol, October 1, 2004; 97(4): 1268 - 1274.
[Abstract] [Full Text] [PDF]

Home page
 HypertensionHome page
J. M. Sasser, J. C. Sullivan, A. A. Elmarakby, B. E. Kemp, D. M. Pollock, and J. S. Pollock
Reduced NOS3 Phosphorylation Mediates Reduced NO/cGMP Signaling in Mesenteric Arteries of Deoxycorticosterone Acetate-Salt Hypertensive Rats
Hypertension, May 1, 2004; 43(5): 1080 - 1085.
[Abstract] [Full Text] [PDF]

Home page
 Circ. Res.Home page
X. F. Figueroa, D. L. Paul, A. M. Simon, D. A. Goodenough, K. H. Day, D. N. Damon, and B. R. Duling
Central Role of Connexin40 in the Propagation of Electrically Activated Vasodilation in Mouse Cremasteric Arterioles In Vivo
Circ. Res., April 18, 2003; 92(7): 793 - 800.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Heart Circ. Physiol.Home page
J. C. Sullivan, A. D. Giulumian, D. M. Pollock, L. C. Fuchs, and J. S. Pollock
Functional NOS 1 in the rat mesenteric arterial bed
Am J Physiol Heart Circ Physiol, August 1, 2002; 283(2): H658 - H663.
[Abstract] [Full Text] [PDF]

Home page
 Eur Heart J SupplHome page
P.M. Vanhoutte
Ageing and endothelial dysfunction
Eur. Heart J. Suppl., February 1, 2002; 4(suppl_A): A8 - A17.
[Abstract] [PDF]


Disclaimer: Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.