AJP - Cell Physiology, Vol 269, Issue 4 C863-C869, Copyright © 1995 by American Physiological Society

ARTICLES

Flow-mediated NO release from endothelial cells is independent of K+ channel activation or intracellular Ca2+

W. C. O'Neill
Department of Medicine, Emory University School of Medicine, Atlanta, Georgia 30322, USA.

The role of K+ channels and intracellular [Ca2+] in flow-induced nitric oxide (NO) production was investigated in bovine aortic endothelial cells in culture. NO release (measured as nitrite production) and K+ channel activity (measured as 86Rb+ efflux) were measured in cells grown on collagen-coated microcarrier beads and perfused in a column. An eightfold increase in flow produced a rapid (within 1 min), sustained, and reversible sixfold increase in NO release. Efflux of 86Rb+ also increased but rapidly returned to baseline and then transiently decreased when flow was decreased. This was probably due to boundary layer washout rather than to K+ channel activation, because an identical pattern was seen for release of [3H]ouabain. Neither tetraethylammonium nor increasing medium [K+] to block K+ currents prevented flow-induced NO release. Removal of medium Ca2+ or chelation of intracellular Ca2+ also did not block flow-mediated NO release. The results demonstrate that flow rapidly increases NO release from endothelial cells but that this increase in NO release is not dependent on activation of K+ channels or changes in intracellular [Ca2+].

This article has been cited by other articles:

				A. R. Burns, Z. Zheng, S. H. Soubra, J. Chen, and R. E. Rumbaut Transendothelial flow inhibits neutrophil transmigration through a nitric oxide-dependent mechanism: potential role for cleft shear stress Am J Physiol Heart Circ Physiol, November 1, 2007; 293(5): H2904 - H2910. [Abstract] [Full Text] [PDF]

				C. Liu, S. Mather, Y. Huang, C. J. Garland, and X. Yao Extracellular ATP facilitates flow-induced vasodilatation in rat small mesenteric arteries Am J Physiol Heart Circ Physiol, May 1, 2004; 286(5): H1688 - H1695. [Abstract] [Full Text] [PDF]

				G. Vazquez, J.-P. Lievremont, G. St. J. Bird, and J. W. Putney Jr. Human Trp3 forms both inositol trisphosphate receptor-dependent and receptor-independent store-operated cation channels in DT40 avian B lymphocytes PNAS, September 5, 2001; (2001) 201238198. [Abstract] [Full Text] [PDF]

				Z. Ungvari, D. Sun, A. Huang, G. Kaley, and A. Koller Role of endothelial [Ca2+]i in activation of eNOS in pressurized arterioles by agonists and wall shear stress Am J Physiol Heart Circ Physiol, August 1, 2001; 281(2): H606 - H612. [Abstract] [Full Text] [PDF]

				S. H. Nelson, O. S. Steinsland, Y. Wang, C. Yallampalli, Y.-L. Dong, and J. M. Sanchez Increased Nitric Oxide Synthase Activity and Expression in the Human Uterine Artery During Pregnancy Circ. Res., September 1, 2000; 87(5): 406 - 411. [Abstract] [Full Text] [PDF]

				Y. S. Chang, J. A. Yaccino, S. Lakshminarayanan, J. A. Frangos, and J. M. Tarbell Shear-Induced Increase in Hydraulic Conductivity in Endothelial Cells Is Mediated by a Nitric Oxide-Dependent Mechanism Arterioscler. Thromb. Vasc. Biol., January 1, 2000; 20(1): 35 - 42. [Abstract] [Full Text] [PDF]

				T. W. Hein, J. C. Liao, and L. Kuo oxLDL specifically impairs endothelium-dependent, NO-mediated dilation of coronary arterioles Am J Physiol Heart Circ Physiol, January 1, 2000; 278(1): H175 - H183. [Abstract] [Full Text] [PDF]

				Y. Guo, W. K. Jones, Y.-T. Xuan, X.-L. Tang, W. Bao, W.-J. Wu, H. Han, V. E. Laubach, P. Ping, Z. Yang, et al. The late phase of ischemic preconditioning is abrogated by targeted disruption of the inducible NO synthase gene PNAS, September 28, 1999; 96(20): 11507 - 11512. [Abstract] [Full Text] [PDF]

				M. P. Boric, X. F. Figueroa, M. V. Donoso, A. Paredes, I. Poblete, and J. P. Huidobro-Toro Rise in endothelium-derived NO after stimulation of rat perivascular sympathetic mesenteric nerves Am J Physiol Heart Circ Physiol, September 1, 1999; 277(3): H1027 - H1035. [Abstract] [Full Text] [PDF]

				I. Fleming, J. Bauersachs, B. Fisslthaler, and R. Busse Ca2+-Independent Activation of the Endothelial Nitric Oxide Synthase in Response to Tyrosine Phosphatase Inhibitors and Fluid Shear Stress Circ. Res., April 6, 1998; 82(6): 686 - 695. [Abstract] [Full Text] [PDF]

				J. Hoyer, R. Köhler, and A. Distler Mechanosensitive Ca2+ oscillations and STOC activation in endothelial cells FASEB J, March 1, 1998; 12(3): 359 - 366. [Abstract] [Full Text]

				G. Garcia-Cardena, R. Fan, D. F. Stern, J. Liu, and W. C. Sessa Endothelial Nitric Oxide Synthase Is Regulated by Tyrosine Phosphorylation and Interacts with Caveolin-1 J. Biol. Chem., November 1, 1996; 271(44): 27237 - 27240. [Abstract] [Full Text] [PDF]

				M. A. Corson, N. L. James, S. E. Latta, R. M. Nerem, B. C. Berk, and D. G. Harrison Phosphorylation of Endothelial Nitric Oxide Synthase in Response to Fluid Shear Stress Circ. Res., November 1, 1996; 79(5): 984 - 991. [Abstract] [Full Text]

				K. Ayajiki, M. Kindermann, M. Hecker, I. Fleming, and R. Busse Intracellular pH and Tyrosine Phosphorylation but Not Calcium Determine Shear Stress–Induced Nitric Oxide Production in Native Endothelial Cells Circ. Res., May 1, 1996; 78(5): 750 - 758. [Abstract] [Full Text]

				P. Palestini, C. Calvi, E. Conforti, L. Botto, C. Fenoglio, and G. Miserocchi Composition, biophysical properties, and morphometry of plasma membranes in pulmonary interstitial edema Am J Physiol Lung Cell Mol Physiol, June 1, 2002; 282(6): L1382 - L1390. [Abstract] [Full Text] [PDF]