Evidence that renal arginine transport is impaired in spontaneously hypertensive rats

N. W. Rajapakse, S. Kuruppu, I. Hanchapola, K. Venardos, D. L. Mattson, A. I. Smith, D. M. Kaye, R. G. Evans

Research output: Contribution to journalArticle

Abstract

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 superim-position of L-arginine (100 μmol·kg-1·min-1; 30 min), the NO synthase inhibitor N G-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 super imposition 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.

Original languageEnglish (US)
Pages (from-to)F1554-F1562
JournalAmerican Journal of Physiology - Renal Physiology
Volume302
Issue number12
DOIs
StatePublished - Jun 15 2012
Externally publishedYes

Fingerprint

Inbred SHR Rats
Arginine
Kidney
Nitric Oxide
Lysine
Sprague Dawley Rats
Perfusion
Biological Availability
Hypertension
Laser-Doppler Flowmetry
Nitric Oxide Donors
Nitroprusside
Nitric Oxide Synthase
Maintenance

Keywords

  • Hypertension
  • Kidney
  • L-arginine transport
  • Nitric oxide

ASJC Scopus subject areas

  • Physiology
  • Urology

Cite this

Rajapakse, N. W., Kuruppu, S., Hanchapola, I., Venardos, K., Mattson, D. L., Smith, A. I., ... Evans, R. G. (2012). Evidence that renal arginine transport is impaired in spontaneously hypertensive rats. American Journal of Physiology - Renal Physiology, 302(12), F1554-F1562. https://doi.org/10.1152/ajprenal.00084.2011

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.; Evans, R. G.

In: American Journal of Physiology - Renal Physiology, Vol. 302, No. 12, 15.06.2012, p. F1554-F1562.

Research output: Contribution to journalArticle

Rajapakse, NW, Kuruppu, S, Hanchapola, I, Venardos, K, Mattson, DL, Smith, AI, Kaye, DM & Evans, RG 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. https://doi.org/10.1152/ajprenal.00084.2011
Rajapakse, N. W. ; Kuruppu, S. ; Hanchapola, I. ; Venardos, K. ; Mattson, D. L. ; Smith, A. I. ; Kaye, D. M. ; Evans, R. G. / Evidence that renal arginine transport is impaired in spontaneously hypertensive rats. In: American Journal of Physiology - Renal Physiology. 2012 ; Vol. 302, No. 12. pp. F1554-F1562.
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