| |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Integrative Physiology |
From the Department of Medical Physics, University of Amsterdam, Academic Medical Center, Amsterdam, The Netherlands.
Correspondence to Dr Ed VanBavel, Dept of Medical Physics, University of Amsterdam, Academic Medical Center, PO Box 22700, 1100 DE Amsterdam, The Netherlands. E-mail e.vanbavel{at}amc.uva.nl
Coronary blood vessels are compressed by the contracting myocardium. This leads to oscillations in flow in especially the subendocardium. We examined the effects of steady and oscillating flow on isolated, cannulated subendocardial and subepicardial porcine arterioles. Steady flowinduced dilation in both vessel types, up to 12.9±0.8% of the passive diameter in subendocardials and 9.6±1.4% in subepicardials at 40 dyne/cm2. Dilation was completely abolished after treatment with 10 µmol/L L-NNA. Sinusoidal modulation of steady flow at 1.5 Hz and 50% to 200% amplitude did not affect dilation. Oscillating flow without a net forward component with peak-peak shear values up to 100 dyne/cm2 caused no dilation at all in these vessels. However, in the presence of 100 U/mL superoxide dismutase (SOD), oscillating flow induced dilation up to 19.5±2.3% in subendocardial vessels and 11.5±4.3% in subepicardials. LNNA (10 µmol/L) blocked this dilation by approximately 50%. SOD did not affect the magnitude of steady flow-induced dilation, but the response time after onset of steady flow shortened from 23.4±1.5 to 14.3±2.1 seconds. Diphenyleneiodinium, an inhibitor of NAD(P)H oxidase, uncovered dilation to oscillating flow in subendocardial vessels up to 9.5±1.6%. Flow causes production of both NO and O2-. During steady flow, the bioavailability of NO is sufficient to cause vasodilation. During oscillating flow, NO is quenched by the O2-, suppressing vasodilation. Considering the pulsatile nature of subendocardial flow and the vulnerability of this layer, pharmacological manipulation of the balance between NO and O2- may improve subendocardial perfusion.
Key Words: flow-induced dilation coronary arterioles oxidative stress oscillating flow superoxide dismutase
This article has been cited by other articles:
![]() |
L. S. Kang, R. A. Reyes, and J. M. Muller-Delp Aging impairs flow-induced dilation in coronary arterioles: role of NO and H2O2 Am J Physiol Heart Circ Physiol, September 1, 2009; 297(3): H1087 - H1095. [Abstract] [Full Text] [PDF] |
||||
![]() |
K. E. Pyke, V. Poitras, and M. E. Tschakovsky Brachial artery flow-mediated dilation during handgrip exercise: evidence for endothelial transduction of the mean shear stimulus Am J Physiol Heart Circ Physiol, June 1, 2008; 294(6): H2669 - H2679. [Abstract] [Full Text] [PDF] |
||||
![]() |
O. Sorop, D. Merkus, V. J. de Beer, B. Houweling, A. Pistea, E. O. McFalls, F. Boomsma, H. M. van Beusekom, W. J. van der Giessen, E. VanBavel, et al. Functional and Structural Adaptations of Coronary Microvessels Distal to a Chronic Coronary Artery Stenosis Circ. Res., April 11, 2008; 102(7): 795 - 803. [Abstract] [Full Text] [PDF] |
||||
![]() |
R. F. Kelly and H. M. Snow Characteristics of the response of the iliac artery to wall shear stress in the anaesthetized pig J. Physiol., July 15, 2007; 582(2): 731 - 743. [Abstract] [Full Text] [PDF] |
||||
![]() |
N. Duerrschmidt, C. Stielow, G. Muller, P. J. Pagano, and H. Morawietz NO-mediated regulation of NAD(P)H oxidase by laminar shear stress in human endothelial cells J. Physiol., October 15, 2006; 576(2): 557 - 567. [Abstract] [Full Text] [PDF] |
||||
![]() |
N. Westerhof, C. Boer, R. R. Lamberts, and P. Sipkema Cross-talk between cardiac muscle and coronary vasculature. Physiol Rev, October 1, 2006; 86(4): 1263 - 1308. [Abstract] [Full Text] [PDF] |
||||
![]() |
S. Lehoux Redox signalling in vascular responses to shear and stretch Cardiovasc Res, July 15, 2006; 71(2): 269 - 279. [Abstract] [Full Text] [PDF] |
||||
![]() |
A. Pistea, E. N. T. P. Bakker, J. A. E. Spaan, and E. VanBavel Flow inhibits inward remodeling in cannulated porcine small coronary arteries Am J Physiol Heart Circ Physiol, December 1, 2005; 289(6): H2632 - H2640. [Abstract] [Full Text] [PDF] |
||||
![]() |
E. A. Koop, M. F. B. G. Gebbink, T. E. Sweeney, M.-J. Mathy, H. F. G. Heijnen, J. A. E. Spaan, E. E. Voest, E. VanBavel, and S. L. M. Peters Impaired flow-induced dilation in mesenteric resistance arteries from receptor protein tyrosine phosphatase-{micro}-deficient mice Am J Physiol Heart Circ Physiol, March 1, 2005; 288(3): H1218 - H1223. [Abstract] [Full Text] [PDF] |
||||
![]() |
X Lu and G. S Kassab Nitric oxide is significantly reduced in ex vivo porcine arteries during reverse flow because of increased superoxide production J. Physiol., December 1, 2004; 561(2): 575 - 582. [Abstract] [Full Text] [PDF] |
||||
![]() |
M. B. Dancu, D. E. Berardi, J. P. Vanden Heuvel, and J. M. Tarbell Asynchronous Shear Stress and Circumferential Strain Reduces Endothelial NO Synthase and Cyclooxygenase-2 but Induces Endothelin-1 Gene Expression in Endothelial Cells Arterioscler Thromb Vasc Biol, November 1, 2004; 24(11): 2088 - 2094. [Abstract] [Full Text] [PDF] |
||||
|
Circulation Research Home | Subscriptions | Archives | Feedback | Authors | Help | AHA Journals Home | Search Copyright © 2003 American Heart Association, Inc. All rights reserved. Unauthorized use prohibited. |