HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) All Versions of this Article: 288/3/H1257    most recent 00856.2004v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Web of Science (3) Citing Articles via Google Scholar Google Scholar Articles by Lominadze, D. Articles by D'Souza, S. E. Search for Related Content PubMed PubMed Citation Articles by Lominadze, D. Articles by D'Souza, S. E.

Fibrinogen and fragment D-induced vascular constriction

Department of Physiology and Biophysics, Health Sciences Center, University of Louisville, Kentucky

Submitted 20 August 2004 ; accepted in final form 5 November 2004

Elevated fibrinogen (Fg) concentration in blood is a high risk factor for many cardiovascular diseases. We hypothesize that Fg and its early degradation product, fragment D, may result in arterial constriction by binding endothelial intercellular adhesion molecule-1 (ICAM-1). The vasoconstriction induced by Fg and fragment D was studied in third- and second-order arterioles (3As and 2As, respectively) of Sprague-Dawley rat cremaster muscle in vivo, in aortic and femoral artery rings, and in the segments of first-order arterioles (1As) isolated from rat cremaster muscle. Intravascular infusion of Fg induced significant constriction of 3As and 2As (by 33.4 ± 3.4 and 23.7 ± 4.3%, respectively) in vivo and was abolished in the presence of the specific endothelin type A receptor blocker BQ-610. Fg and fragment D produced significant constriction of both aortic and femoral artery rings. Isolated 1As constricted in response to Fg (0.3 µM) and fragment D (3 µM) by 31 ± 1.4 and 12 ± 1.5%, respectively. Fluorescently labeled Fg and fragment D bound to the vascular wall, whereas albumin bound to a significantly lesser degree. The binding of Fg and fragment D to the arteriolar wall and constriction of aortic and femoral artery rings as well as isolated 1As were abolished in the presence of anti-Fg and anti-ICAM-1 antibodies. These results indicate that binding of Fg and fragment D to the vascular wall through ICAM-1 may contribute to the increased vascular tone and resistance that compromise circulation.

arteries; endothelin; endothelium; intercellular adhesion molecule-1

This article has been cited by other articles:

				S. Kim and J. A. Nadel Fibrinogen binding to ICAM-1 promotes EGFR-dependent mucin production in human airway epithelial cells Am J Physiol Lung Cell Mol Physiol, July 1, 2009; 297(1): L174 - L183. [Abstract] [Full Text] [PDF]

				U. Sen, N. Tyagi, P. K. Patibandla, W. L. Dean, S. C. Tyagi, A. M. Roberts, and D. Lominadze Fibrinogen-induced endothelin-1 production from endothelial cells Am J Physiol Cell Physiol, April 1, 2009; 296(4): C840 - C847. [Abstract] [Full Text] [PDF]