This Article Full Text Full Text (PDF) 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 PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Christopher, J. Articles by Jaffa, A. A. Search for Related Content PubMed PubMed Citation Articles by Christopher, J. Articles by Jaffa, A. A.

(Hypertension. 2001;38:602.)
© 2001 American Heart Association, Inc.

Cardiovascular Biology

Induction of B₁-Kinin Receptors in Vascular Smooth Muscle Cells: Cellular Mechanisms of MAP Kinase Activation

Julie Christopher; Victoria Velarde; Ayad A. Jaffa

Department of Medicine and Cell and Molecular Pharmacology and Experimental Therapeutics, Medical University of South Carolina (J.C., A.A.J.), Charleston; and Deparmento de Ciencias Fisiológicas, Facultad de Ciencias Biológicas, Pontificia Universidad Católica de Chile (V.V.), Chile.

Correspondence to Ayad A Jaffa, PhD, Associate Professor of Medicine, Endocrinology-Diabetes–Medical Genetics, Medical University of South Carolina, 114 Doughty St, Charleston, SC 29425. E-mail jaffaa{at}musc.edu

Abstract

Abstract—— Vascular smooth muscle cell (VSMC) proliferation is a prominent feature of the atherosclerotic process that occurs after endothelial injury. Although a vascular wall kallikrein-kinin system has been described, its contribution to vascular disease remains undefined. Because the B₁-kinin receptor subtype (B1KR) is induced in VSMCs only in response to injury, we hypothesize that this receptor may be mediating critical events in the progression of vascular disease. In the present study, we provide evidence that des-Arg⁹-bradykinin (dABK) (10^-8 M), acting through B1KR, stimulates the phosphorylation of mitogen-activated protein kinase (MAPK) (p42^mapk and p44^mapk). Activation of MAPK by dABK is mediated via a cholera toxin–sensitive pathway and appears to involve protein kinase C, Src kinase, and MAPK kinase. These findings demonstrate that the activation of B1KR in VSMCs leads to the generation of second messengers that converge to activate MAPK and provide a rationale to investigate the mitogenic actions of dABK in vascular injury.

Key Words: receptors, kinin, B₁ • protein kinases • muscle, smooth, vascular

This article has been cited by other articles:

				G. S. Ceravolo, L. Fernandes, C. D. Munhoz, D. C. Fernandes, R. C.A. Tostes, F. R.M. Laurindo, C. Scavone, Z. B. Fortes, and M. H. C. Carvalho Angiotensin II Chronic Infusion Induces B1 Receptor Expression in Aorta of Rats Hypertension, October 1, 2007; 50(4): 756 - 761. [Abstract] [Full Text] [PDF]

				L. M. F. Leeb-Lundberg, F. Marceau, W. Muller-Esterl, D. J. Pettibone, and B. L. Zuraw International Union of Pharmacology. XLV. Classification of the Kinin Receptor Family: from Molecular Mechanisms to Pathophysiological Consequences Pharmacol. Rev., March 1, 2005; 57(1): 27 - 77. [Abstract] [Full Text] [PDF]

				T. Ignjatovic, S. Stanisavljevic, V. Brovkovych, R. A. Skidgel, and E. G. Erdos Kinin B1 Receptors Stimulate Nitric Oxide Production in Endothelial Cells: Signaling Pathways Activated by Angiotensin I-Converting Enzyme Inhibitors and Peptide Ligands Mol. Pharmacol., November 1, 2004; 66(5): 1310 - 1316. [Abstract] [Full Text] [PDF]