title: Advective transport of nitric oxide in a mathematical model of the afferent arteriole.
abstract: 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.
authors.affiliation: Department of Mathematics, Suke University , Durham, North Carolina 27708-0320, USA.
authors.forename: Kayne M
authors.initials: KM
authors.lastname: Smith
authors.forename: Leon C
authors.initials: LC
authors.lastname: Moore
authors.forename: Harold E
authors.initials: HE
authors.lastname: Layton
mesh_terms: D000818:Animals; D001160:Arterioles / Q000502:physiology*; D001692:Biological Transport; D003198:Computer Simulation; D006801:Humans; D008955:Models, Cardiovascular; D009569:Nitric Oxide / Q000097:blood / Q000378:metabolism*; D014661:Vasoconstriction / Q000502:physiology; D014664:Vasodilation / Q000502:physiology
chemical_list: D009569:Nitric Oxide