|
| HOME | SUBSCRIPTIONS | CURRENT ISSUE | PAST ISSUES | CARDIOSOURCE | SEARCH | HELP | FEEDBACK |
|
|
|
|||||||||
|
|||||||||||
|
J Am Coll Cardiol, 2000; 36:1467-1473 © 2000 by the American College of Cardiology Foundation |
a Cardiology Branch, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland, USA
Manuscript received May 11, 1999; revised manuscript received April 20, 2000, accepted June 19, 2000.
Reprint requests and correspondence: Dr. Arshed A. Quyyumi, National Institutes of Health, Cardiology Branch, NHLBI, Bldg. 10, Rm. 7B15, 10 Center Dr. MSC 1650, Bethesda, Maryland 20892-1650
quyyumia{at}nih.gov
OBJECTIVES
The aim of our study was to investigate coronary vascular kinin receptor function in patients with atherosclerosis or its risk factors.
BACKGROUND
Although acetylcholine (ACH) is used as a probe for testing vascular function in vivo, endogenous bradykinin (BK) regulates resting and flow-mediated epicardial tone.
METHODS
In 53 patients with mild atherosclerosis or its risk factors and 9 control subjects, endothelium-dependent vasomotion was tested with intracoronary ACH (30 µg/min) and BK (62.5 ng/min and 4 µg/min), and endothelium-independent function with sodium nitroprusside. Metabolic vasodilation was assessed during cardiac pacing (n = 19). Correlation with serum angiotensin-converting enzyme (ACE) levels and the ACE insertion/deletion genotype was performed.
RESULTS
There was progressive impairment in ACH-mediated microvascular dilation with increasing numbers of risk factors (p = 0.025, analysis of variance). By contrast, BK- and sodium nitroprusside-mediated microvascular dilation was similar in all groups. Similarly, there was no correlation between epicardial coronary responses to ACH and BK; segments that constricted or dilated with ACH had similar dilator responses with BK. Bradykinin, but not ACH-mediated vasomotion, was depressed in epicardial segments that constricted with pacing. Finally, epicardial BK responses were depressed in patients with high ACE levels and in those with the ACE DD genotype.
CONCLUSIONS
Endothelial dysfunction in atherosclerosis appears to be receptor-specific, involving the muscarinic receptor with relative sparing of the kinin receptor pathways. Abnormal reactivity of epicardial coronary arteries during physiologic stress is better represented by BK and not by ACH responses. Bradykinin activity and, hence, physiologic coronary vasomotion appears to be influenced by serum ACE levels and the ACE insertion/deletion genotype.
| ||||||||||||||||||||
This article has been cited by other articles:
|
|
 |
|
  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]
|
|
|
|
 |
|
 J. P.J. Halcox, W. H. Schenke, G. Zalos, R. Mincemoyer, A. Prasad, M. A. Waclawiw, K. R.A. Nour, and A. A. Quyyumi Prognostic Value of Coronary Vascular Endothelial Dysfunction Circulation, August 6, 2002; 106(6): 653 - 658. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J. P. J. Halcox, S. Narayanan, L. Cramer-Joyce, R. Mincemoyer, and A. A. Quyyumi Characterization of endothelium-derived hyperpolarizing factor in the human forearm microcirculation Am J Physiol Heart Circ Physiol, June 1, 2001; 280(6): H2470 - H2477. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 A. Prasad, S. Narayanan, M. A. Waclawiw, N. Epstein, and A. A. Quyyumi The insertion/deletion polymorphism of the angiotensin-converting enzyme gene determines coronary vascular tone and nitric oxide activity J. Am. Coll. Cardiol., November 1, 2000; 36(5): 1579 - 1586. [Abstract] [Full Text] [PDF]
|
|
| HOME | SUBSCRIPTIONS | CURRENT ISSUE | PAST ISSUES | CARDIOSOURCE | SEARCH | HELP | FEEDBACK |
