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Fluid flow stimulates rapid and continuous release of nitric oxide in osteoblastsInterstitial fluid flow may mediate skeletal remodeling in response to mechanical loading. Because nitric oxide (NO) has been shown to be an osteoblast mitogen and inhibitor of osteoclastic resorption, we investigated and characterized the role of fluid shear on the release of NO in osteoblasts. Rat calvarial cells in a stationary culture produced undetectable levels of NO. Fluid shear stress (6 dyn/cm2) rapidly increased NO release rate to 9.8 nmol.h-1.mg protein-1 and sustained this production for 12 h of exposure to flow. Cytokine treatment also induced NO synthesis after a 12-h lag phase of zero production, followed by a production rate of 0.6 nmol.h-1.mg protein-1. Flow-induced NO production was blocked by the NO synthase (NOS) inhibitor NG-amino-L-arginine, but not by dexamethasone, which suggests that the flow stimulated a constitutive NOS isoform. This is the first time that a functional constitutively present NOS isoform has been identified in osteoblasts. Moreover, fluid flow represents the most potent stimulus of NO release in osteoblasts reported to date. Fluid flow-induced NO production may therefore play a primary role in bone maintenance and remodeling.
Document ID
20040173184
Acquisition Source
Legacy CDMS
Document Type
Reprint (Version printed in journal)
Authors
Johnson, D. L.
(University of California San Diego, La Jolla 92093, United States)
McAllister, T. N.
Frangos, J. A.
Date Acquired
August 22, 2013
Publication Date
July 1, 1996
Publication Information
Publication: The American journal of physiology
Volume: 271
Issue: 1 Pt 1
ISSN: 0002-9513
Subject Category
Life Sciences (General)
Distribution Limits
Public
Copyright
Other
Keywords
NASA Discipline Cell Biology
Non-NASA Center

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