Summary
Endothelial cells produce a variety of factors involved in the control of vascular tone, platelet activation and cell growth, one of the most important being nitric oxide (NO). Although continuously produced in small amounts by the endothelium, various physical and humoral stimuli greatly enhance the release of NO. The physiologically most important stimulus for the release of NO from these cells is considered to be the shear stress (or viscous drag) exerted on the luminal surface of the endothelium by the streaming blood. This stimulus does not only affect NO production acutely, but may also be required to maintain endothelial NO synthase expression. This brief overview resumes current knowledge on the potential mechanisms involved both in the acute and long-term effects of shear stress on endothelial NO formation.
Access this chapter
Tax calculation will be finalised at checkout
Purchases are for personal use only
Preview
Unable to display preview. Download preview PDF.
Similar content being viewed by others
References
Bhagyalakshmi, A., F. Berthiaume, K.M. Reich and J.A. Frangos, 1992. Fluid shear stress stimulates membrane phospholipid metabolism in cultured human endothelial cells, J. Vasc. Res. 29, 443.
Busse, R., A. Mülsch, I. Fleming and M. Hecker, 1993. Mechanisms of nitric oxide release from the vascular endothelium. Circulation 87, V18.
Busse, R., M. Hecker and I. Fleming, 1994. Control of nitric oxide and prostacyclin synthesis in endothelial cells. Arzneim. Forsch./Drug Res. 44, 392.
Creager, M.A., J.P. Cooke, M.E. Mendelsohn, S.J. Gallagher, S.M. Coleman, J. Loscalzo and V.H. Dzau, 1990. Impaired vasodilation of forearm resistance vessels in hypercholesterolemic humans, J. Clin. Invest. 86, 228.
Cooke, J. P., E. Rossitch, N. A. Andon, J. Loscalzo and V. J. Dzau, 1991. Flow activates an endothelial potassium channel to release an endogenous nitrovasodilator, J. Clin. Invest. 88, 1663.
Falcone, J.C., L. Kuo and G.A. Meininger, 1993. Endothelial cell calcium increases during flow-induced dilation in isolated arterioles. Am. J. Physiol. 264, H653.
Fleming, I., M. Hecker and R. Busse, 1994. Intracellular alkalinisation induced by bradykinin sustains activation of the constitutive nitric oxide synthase in endothelial cells. Circ. Res., in press.
Geiger, R. V., B. C. Berk, R. W. Alexander and R. M. Nerem, 1992. Flow-induced calcium transients in single endothelial cells: spatial and temporal analysis, Am. J. Physiol. 262, C1411.
Golino, P., F. Piscione, J.T. Willerson, M. Cappellibigazzi, A. Focaccio, B. Villari, C. Indolfi, E. Russolillo, M. Condorelli and M. Chiarello, 1991. Divergent effects of serotonin on coronary artery dimensions and blood flow in patients with coronary atherosclerosis and control patients, N. Engl. J. Med. 324, 641.
Griffith, T. M. and D. H. Edwards, 1990. Myogenic autoregulation of flow may be inversely related to endothelium-derived relaxing factor activity, Am. J. Physiol. 258, H1171.
Hecker, M., A. Mülsch, E. Bassenge and R. Busse, 1993. Vasoconstriction and increased flow: Two principal mechanisms of shear stress-dependent endothelial autacoid release. Am. J. Physiol. 265, H828.
Hecker, M., A. Mülsch, E. Bassenge, U. Forstermann and R. Busse, 1994. Subcellular localisation and characterization of nitric oxide synthase(s) in endothelial cells -physiologic implications. Biochem. J. 299, 247.
Kubo, S.H., T.S. Rector, A.J. Bank, R.E. Williams and S.M. Heifetz, 1991. Endothelium-dependent vasodilation is attenuated in patients with heart failure, Circulation 84, 1589.
Lamontagne, D., U. Pohl and R. Busse, 1992. Mechanical deformation of vessel wall and shear stress determine the basal EDRF release in the intact coronary vascular bed, Circ. Res. 70, 123.
Linder, L. W. Kiowski, F.R. Bühler and T.F. Lüscher, 1990. Indirect evidence for release of endothelium-derived relaxing factor in human forearm circulation in vivo -blunted response in essential hypertension, Circulation 81, 1762.
Lückhoff, A. and R. Busse, 1990. Activators of potassium channels enhance calcium influx into endothelial cells as a consequence of potassium currents, Naunyn-Schmiedebeg’s Arch. Pharmacol. 342, 94.
Macarthur, H., M. Hecker, R. Busse and J.R. Vane, 1993. Selective inhibition of agonist-induced but not shear stress-dependent endothelial autacoid release by thapsigargin. Br. J. Pharmacol. 108, 100.
Melkumyants, A.M., S.A. Balashov and V.M. Khayutin, 1989. Endothelium dependent control of arterial diameter by blood viscosity, Cardiovasc. Res. 23, 741.
Mo, M., S. G. Eskin and W. P. Schilling, 1991. Flow-induced changes in Ca2+ signaling of vascular endothelial cells -effect of shear stress and ATP, Am. J. Physiol. 260, H1698.
Nadaud, S., A. Bonnardeaux, M. Lathrop and F. Soubrier, 1994. Gene structure, polymorphism and mapping of the human endothelial nitric oxide synthase gene, Biochem. Biophys. Res. Commun. 198, 1027.
Nishida, K., D.G. Harrison, J.P. Navas, A.A, Fisher, S.P. Dockery, M. Uematsu, R.M. Nerem, R.W. Alexander and T.J. Murphy, 1992. Molecular cloning and characterization of the constitutive bovine aortic endothelial cell nitric oxide synthase, J. Clin. Invest. 90, 2092.
Nollert, M.U., S.G. Eskin and L.V. McIntyre, 1990. Shear stress increases inositol trisphosphate levels in human endothelial cells, Biochem. Biophys. Res. Commun. 170, 281.
Nollert, M.U., N.J. Panaro and L.V. McIntire, 1992. Regulation of genetic expression in shear stress-stimulated endothelial cells, Ann. N. Y. Acad. Sci. 665, 94.
Olesen, S. P., D. E. Clapham and P. F. Davies, 1988. Haemodynamic shear stress activates a K+ current in vascular endothelial cells, Nature 331, 168.
Pohl, U., K. Herlan, A. Huang and E. Bassenge, 1991. EDRF-mediated shear-induced dilation opposes myogenic vasoconstriction in small rabbit arteries, Am. J. Physiol. 261, H2016.
Prasad, A.R.S., S.A. Logan, R.M. Nerem, C.J. Schwartz and E.A. Sprague, 1993. Flow-related responses of intracellular inositol phosphate levels in cultured aortic endothelial cells, Circ. Res. 72, 827.
Schwarz, G., G. Callewaert, G. Droogmans and B. Nilius, 1992. Shear stress induced calcium transients in endothelial cells from human umbilical cord veins, J. Physiol. (Lond.) 458, 527.
Sessa, W.C., K. Pritchard, N. Seyedi, J. Wang and T.H. Hintze, 1994. Chronic exercise in dogs increases coronary vascular nitric oxide production and endothelial cell nitric oxide synthase gene expression, Circ. Res. 74, 349.
Shen, J., F. W. Luscinskas, A. Connolly, C. F. Dewey and M. A. Gimbrone, 1992. Fluid shear stress modulates cytosolic free calcium in vascular endothelial cells, Am. J. Physiol. 262, C384.
Uematsu, , M., J.P. Navas, K. Nishida, Y. Ohara, T.J. Murphy, R.W. Alexander, R.M. Nerem and D.G. Harrison, 1993. Mechanisms of endothelial cell NO synthase induction by shear stress, Circulation 88, I–184.
Vita, J.A., C.B. Treasure, P. Ganz, D.A. Fox, R.D. Fish and A.P. Selwyn, 1989. Control of shear stress in the epicardial coronary arteries of humans -impairment by atherosclerosis, J. Am. Coll. Cardiol. 14, 1193.
Watson, P.A., 1991. Function follows form: generation of intracellular signals by cell deformation, FASEB J. 5, 2013.
Zeiher, A.M., H. Drexler, H. Wollschlager and H. Just, 1991. Modulation of coronary vasomotor tone in humans -progressive endothelial dysfunction with different early stages of coronary atherosclerosis, Circulation 83, 391.
Ziegelstein, R.C., L. Cheng and M.C. Capogrossi, 1992. Flow-dependent cytosolic acidification of vascular endothelial cells, Science 258, 656.
Author information
Authors and Affiliations
Editor information
Editors and Affiliations
Rights and permissions
Copyright information
© 1995 Springer Science+Business Media New York
About this chapter
Cite this chapter
Hecker, M., Fleming, I., Ayajiki, K., Busse, R. (1995). Mechanisms of Shear Stress-Dependent Endothelial Nitric Oxide Release: Cardiovascular Implications. In: Weissman, B.A., Allon, N., Shapira, S. (eds) Biochemical, Pharmacological, and Clinical Aspects of Nitric Oxide. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-1903-4_5
Download citation
DOI: https://doi.org/10.1007/978-1-4615-1903-4_5
Publisher Name: Springer, Boston, MA
Print ISBN: 978-1-4613-5777-3
Online ISBN: 978-1-4615-1903-4
eBook Packages: Springer Book Archive