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Am J Physiol Renal Physiol 284: F1080-F1096, 2003. First published January 7, 2003; doi:10.1152/ajprenal.00141.2002
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Vol. 284, Issue 5, F1080-F1096, May 2003

Advective transport of nitric oxide in a mathematical model of the afferent arteriole

Kayne M. Smith1, Leon C. Moore2, and Harold E. Layton1

1 Department of Mathematics, Duke University, Durham, North Carolina 27708-0320; and 2 Department of Physiology and Biophysics, State University of New York, Stony Brook, New York 11794-8661

Endothelium-derived nitric oxide (NO) is thought to be short-lived in blood because of rapid removal from plasma, mainly by binding to Hb. The extent to which removal limits NO advection is unclear, especially for blood flow in the renal afferent arteriole (AA), which has a transit time of 3-30 ms. A mathematical model of AA fluid dynamics and myogenic response that includes NO diffusion, advection, degradation, and vasorelaxant action was used to estimate NO advective transport. Model simulations indicate that advective transport of locally produced NO is sufficient to yield physiologically significant NO concentrations along much of the AA. Advective transport is insensitive to NO scavenging by Hb because the NO-Hb binding rate is slow relative to AA transit time. Hence, plasma NO concentration near the vessel wall is influenced by both diffusion from endothelial cells and advection from upstream sites. Simulations also suggest that NO advection may constitute a mechanism to stabilize arteriolar flow in response to a localized vasoconstriction accompanied by enhanced NO release.

kidney; renal hemodynamics; myogenic mechanism; immersed boundary method


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