This Article 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 Candipan, R. C. Articles by Cooke, J. P. Search for Related Content PubMed PubMed Citation Articles by Candipan, R. C. Articles by Cooke, J. P.

Circulation, Vol 89, 777-784, Copyright © 1994 by American Heart Association

ARTICLES

Vascular injury augments adrenergic neurotransmission

RC Candipan, PT Hsiun, R Pratt and JP Cooke
Division of Cardiovascular Medicine, Stanford University School of Medicine, Calif.

BACKGROUND: We have observed persistent desensitization to exogenous norepinephrine after balloon injury. We postulated that this desensitization may be due to a local increase in the release of neuronal norepinephrine. METHODS AND RESULTS: New Zealand White rabbits underwent left iliac artery angioplasty; 4 weeks later, both iliac arteries were harvested. Maximal response to exogenous norepinephrine was reduced in injured compared with noninjured vessels (12.3 +/- 1.0 g versus 10.3 +/- 1.5 g; n = 7, P = .056). By contrast, response to electrical stimulation (to induce neuronal norepinephrine release) was significantly greater in injured tissues (36 +/- 7% versus 14 +/- 3%; values expressed as percent of maximal contraction to exogenous norepinephrine; P = .025). Direct measurement of tissue norepinephrine revealed a threefold increase 4 weeks after injury (1236 +/- 410 versus 466 +/- 97 pg/mg; injured versus noninjured). To determine if desensitization to exogenous norepinephrine was due to a persistent increase in neuronal norepinephrine release, the experiments were repeated after chemical sympatholysis using 6-hydroxydopamine (6-OHDA) (65 mg/kg). To determine if activation of vascular angiotensin II contributed to facilitation of adrenergic neurotransmission, other animals received ramipril (RAM; 1 mg/kg per day). Both treatments were initiated 7 days before angioplasty. In the 6-OHDA group there was no evidence of desensitization, judged by maximal response to exogenous norepinephrine (7.5 +/- 0.6 versus 7.5 +/- 0.8, noninjured versus injured). Similar results were obtained in RAM animals (9.9 +/- 0.8 versus 9.6 +/- 1.2, noninjured versus injured). CONCLUSIONS: This is the first study to demonstrate enhanced adrenergic neurotransmission after balloon injury. The facilitation of adrenergic neurotransmission may be due to increased local concentrations of angiotensin II and is associated with desensitization to exogenous norepinephrine.

This article has been cited by other articles:

				M. C. Vinci, L. Bellik, S. Filippi, F. Ledda, and A. Parenti Trophic effects induced by {alpha}1D-adrenoceptors on endothelial cells are potentiated by hypoxia Am J Physiol Heart Circ Physiol, October 1, 2007; 293(4): H2140 - H2147. [Abstract] [Full Text] [PDF]

				D. Chalothorn, H. Zhang, J. A. Clayton, S. A. Thomas, and J. E. Faber Catecholamines augment collateral vessel growth and angiogenesis in hindlimb ischemia Am J Physiol Heart Circ Physiol, August 1, 2005; 289(2): H947 - H959. [Abstract] [Full Text] [PDF]

				M. E. Wall, J. E. Faber, X. Yang, M. Tsuzaki, and A. J. Banes Norepinephrine-induced calcium signaling and expression of adrenoceptors in avian tendon cells Am J Physiol Cell Physiol, October 1, 2004; 287(4): C912 - C918. [Abstract] [Full Text] [PDF]

				T. Bleeke, H. Zhang, N. Madamanchi, C. Patterson, and J. E. Faber Catecholamine-Induced Vascular Wall Growth Is Dependent on Generation of Reactive Oxygen Species Circ. Res., January 9, 2004; 94(1): 37 - 45. [Abstract] [Full Text] [PDF]

				C. Erami, H. Zhang, J. G. Ho, D. M. French, and J. E. Faber alpha 1-Adrenoceptor stimulation directly induces growth of vascular wall in vivo Am J Physiol Heart Circ Physiol, October 1, 2002; 283(4): H1577 - H1587. [Abstract] [Full Text] [PDF]

				D. deBlois, S.M. Schwartz, E.M. van Kleef, J.E. Su, K.A. Griffin, A.K. Bidani, M.J.A.P. Daemen, and D.M. Lombardi Chronic {alpha}1-Adrenoreceptor Stimulation Increases DNA Synthesis in Rat Arterial Wall: Modulation of Responsiveness After Vascular Injury Arterioscler. Thromb. Vasc. Biol., September 1, 1996; 16(9): 1122 - 1129. [Abstract] [Full Text]

				R. E. Pratt and V. J. Dzau Pharmacological Strategies to Prevent Restenosis : Lessons Learned From Blockade of the Renin-Angiotensin System Circulation, March 1, 1996; 93(5): 848 - 852. [Full Text]

				H. Zhang, C. S. Facemire, A. J. Banes, and J. E. Faber Different alpha -adrenoceptors mediate migration of vascular smooth muscle cells and adventitial fibroblasts in vitro Am J Physiol Heart Circ Physiol, June 1, 2002; 282(6): H2364 - H2370. [Abstract] [Full Text] [PDF]

				H. Zhang and J. E. Faber Trophic Effect of Norepinephrine on Arterial Intima-Media and Adventitia Is Augmented by Injury and Mediated by Different {alpha}1-Adrenoceptor Subtypes Circ. Res., October 26, 2001; 89(9): 815 - 822. [Abstract] [Full Text] [PDF]