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Am J Physiol Renal Physiol (January 7, 2003). doi:10.1152/ajprenal.00141.2002
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Submitted on April 15, 2002
Accepted on January 2, 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, NC, USA
2 Department of Physiology and Biophysics, State University of New York, Stony Brook, Stony Brook, NY, USA

* To whom correspondence should be addressed. E-mail: layton{at}math.duke.edu.

Endothelium-derived nitric oxide (NO) is thought to be short-lived in blood because of rapid removal from plasma, mainly by binding to hemoglobin (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 included NO diffusion, advection, degradation, and vasorelaxing 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.




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