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Impact of nitric oxide‐mediated vasodilation on outer medullary NaCl transport and oxygenation
Author(s) -
Edwards Aurelie,
Layton Anita T
Publication year - 2012
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.26.1_supplement.1100.6
Subject(s) - vasodilation , reabsorption , chemistry , medullary cavity , nitric oxide , oxygen , medulla , vasoconstriction , renal medulla , medicine , endocrinology , biophysics , kidney , biology , organic chemistry
We expanded our region‐based model of nitric oxide (NO) and superoxide (O2‐) transport in the rat outer medulla to incorporate NO‐mediated vasocontractility of descending vasa recta (DVR). This steady‐state model considers the stimulating and inhibitory effects, respectively, of O2‐ and NO on NaCl reabsorption across the medullary thick ascending limb, and the dilatory effects of NO on DVR. The model is used to examine the impact of NO and O2‐ on NaCl transport and oxygen (O2) consumption, under both physiological and pathological conditions. The model predicts that if the counteracting effects of O2‐ on NaCl reabsorption are blocked, both the outer medullary concentrating capacity and the O2 consumption‐to‐supply ratio decrease more in the presence of NO‐induced vasodilation than in the absence thereof. Conversely, the increase in concentrating capacity and O2 consumption resulting from a ten‐fold increase in O2‐ concentration is amplified by vasoconstriction, since NO levels are then reduced. Our results thus suggest that NO‐mediated vasodilation acts to enhance O2 availability and preserve O2 supply to the inner medulla to the detriment of the concentrating capacity of the outer medulla. This work was supported by National Institutes of Health Grant DK053775.