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

Research output: Contribution to journalArticleResearchpeer-review

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 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
Volume302
Issue number12
DOIs
Publication statusPublished - 2012

Cite this

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title = "Evidence that renal arginine transport is impaired in spontaneously hypertensive rats",
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 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.",
author = "Rajapakse, {Niwanthi W} and Kuruppu, {Don M Sanjaya} and Iresha Hanchapola and Venardos, {Kylie M} and Mattson, {David L} and Smith, {Alexander Ian} and Kaye, {David M} and Evans, {Roger G}",
year = "2012",
doi = "10.1152/ajprenal.00084.2011",
language = "English",
volume = "302",
pages = "F1554 -- F1562",
journal = "American Journal of Physiology - Renal Physiology",
issn = "1522-1466",
publisher = "American Physiological Society",
number = "12",

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Evidence that renal arginine transport is impaired in spontaneously hypertensive rats. / Rajapakse, Niwanthi W; Kuruppu, Don M Sanjaya; Hanchapola, Iresha; Venardos, Kylie M; Mattson, David L; Smith, Alexander Ian; Kaye, David M; Evans, Roger G.

In: American Journal of Physiology - Renal Physiology, Vol. 302, No. 12, 2012, p. F1554 - F1562.

Research output: Contribution to journalArticleResearchpeer-review

TY - JOUR

T1 - Evidence that renal arginine transport is impaired in spontaneously hypertensive rats

AU - Rajapakse, Niwanthi W

AU - Kuruppu, Don M Sanjaya

AU - Hanchapola, Iresha

AU - Venardos, Kylie M

AU - Mattson, David L

AU - Smith, Alexander Ian

AU - Kaye, David M

AU - Evans, Roger G

PY - 2012

Y1 - 2012

N2 - 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.

AB - 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.

UR - http://ajprenal.physiology.org/content/302/12/F1554.full.pdf

U2 - 10.1152/ajprenal.00084.2011

DO - 10.1152/ajprenal.00084.2011

M3 - Article

VL - 302

SP - F1554 - F1562

JO - American Journal of Physiology - Renal Physiology

JF - American Journal of Physiology - Renal Physiology

SN - 1522-1466

IS - 12

ER -