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Evidence that renal arginine transport is impaired in spontaneously hypertensive rats

Rajapakse, N. W., Kuruppu, S., Hanchapola, I., Venardos, K., Mattson, D. L., Smith, A. I., Kaye, D. M. and Evans, R. G. 2012, Evidence that renal arginine transport is impaired in spontaneously hypertensive rats, American journal of physiology - renal physiology, vol. 302, no. 12, pp. F1554-F1562.

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Title Evidence that renal arginine transport is impaired in spontaneously hypertensive rats
Author(s) Rajapakse, N. W.
Kuruppu, S.
Hanchapola, I.
Venardos, K.
Mattson, D. L.
Smith, A. I.
Kaye, D. M.
Evans, R. G.
Journal name American journal of physiology - renal physiology
Volume number 302
Issue number 12
Start page F1554
End page F1562
Total pages 9
Publisher American Physiological Society
Place of publication Bethesda, Md.
Publication date 2012-06-15
ISSN 1931-857X
1522-1466
Keyword(s) hypertension
kidney
L-arginine transport
nitric oxide
Summary Low renal nitric oxide (NO) bioavailability contributes to the development and maintenance of chronic hypertension. We investigated whether impaired L-arginine transport contributes to low renal NO bioavailability in hypertension. Responses of renal medullary perfusion and NO concentration to renal arterial infusions of the L-arginine transport inhibitor L-lysine (10 μmol·kg−1·min−1; 30 min) and subsequent superimposition of L-arginine (100 μmol·kg−1·min−1; 30 min), the NO synthase inhibitor NG-nitro-L-arginine (2.4 mg/kg; iv bolus), and the NO donor sodium nitroprusside (0.24 μg·kg−1·min−1) were examined in Sprague-Dawley rats (SD) and spontaneously hypertensive rats (SHR). Renal medullary perfusion and NO concentration were measured by laser-Doppler flowmetry and polarographically, respectively, 5.5 mm below the kidney surface. Renal medullary NO concentration was less in SHR (53 ± 3 nM) compared with SD rats (108 ± 12 nM; P = 0.004). L-Lysine tended to reduce medullary perfusion (−15 ± 7%; P = 0.07) and reduced medullary NO concentration (−9 ± 3%; P = 0.03) while subsequent superimposition of L-arginine reversed these effects of L-lysine in SD rats. In SHR, L-lysine and subsequent superimposition of L-arginine did not significantly alter medullary perfusion or NO concentration. Collectively, these data suggest that renal L-arginine transport is impaired in SHR. Renal L-[3H]arginine transport was less in SHR compared with SD rats (P = 0.01). Accordingly, we conclude that impaired arginine transport contributes to low renal NO bioavailability observed in the SHR kidney.
Language eng
Field of Research 069999 Biological Sciences not elsewhere classified
Socio Economic Objective 970106 Expanding Knowledge in the Biological Sciences
HERDC Research category C1.1 Refereed article in a scholarly journal
Copyright notice ©2012, the American Physiological Society
Persistent URL http://hdl.handle.net/10536/DRO/DU:30048224

Document type: Journal Article
Collection: School of Life and Environmental Sciences
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