Evidence that renal arginine transport is impaired in spontaneously hypertensive rats

Niwanthi W Rajapakse, Don M Sanjaya Kuruppu, Iresha Hanchapola, Kylie M Venardos, David L Mattson, Alexander Ian Smith, David M Kaye, Roger G Evans

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9 Citations (Scopus)


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 mumol/kg/min; 30 min) and subsequent super-imposition of L-arginine (100 mumol/kg/min; 30 min), the NO synthase inhibitor, N(G)-nitro-L-arginine (2.4 mg/kg; i.v bolus) and the NO donor sodium nitroprusside (0.24 mug/kg/min) 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 super-imposition 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-(3)H-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.
Original languageEnglish
Pages (from-to)F1554 - F1562
Number of pages9
JournalAmerican Journal of Physiology-Renal Physiology
Issue number12
Publication statusPublished - 2012

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