Role of Hemodynamic Alterations in the Partial Protection Afforded by Uninephrectomy against Glycerol-Induced Acute Renal Failure in Rats

Ramos, B.; López‐Novoa, José M.; Hernando, L

doi:10.1159/000182435

Cited by 13 publications

(6 citation statements)

References 17 publications

(24 reference statements)

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“…However, the interpretation of these data is difficult for several reasons. First, arteriovenous differences could not reflect to tal renal uptake, due to the probable decrease in renal plasma flow 36 h after glycerol-in duced ARF [11]. In addition, it has been dem onstrated that the renal cortical metabolism is profoundly influenced by the acid-base status, and this status has been reported to be mod ified during acute uremia [12].…”

Section: Discussionmentioning

confidence: 99%

“…In addition, it has been dem onstrated that the renal cortical metabolism is profoundly influenced by the acid-base status, and this status has been reported to be mod ified during acute uremia [12]. Thus, increased glutamine uptake and ammonia production could be explained by an ARF-associated aci dosis, but, unfortunately, data on acid-base equilibrium were not provided in the study of McFarlane-Anderson et al [11]. In our study, we were able to maintain systemic acid-base equilibrium between normal values during the acute clearance studies in dogs with postischemic ARF.…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Renal Ammoniagenesis during the Recovery Phase of Postischemic Acute Renal Failure in the Dog1

Montañés¹,

Badia²,

Rengel³

et al. 1990

Kidney Blood Press Res

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Renal ammoniagenesis has been studied in 6 dogs before and 48 h after a 60-min period of renal ischemia induced by clamping the renal artery and in 6 sham-operated animals. Two days after temporary renal ischemia, the dogs showed a 25% decrease in glomerular filtration rate and renal plasma flow and a similar decrease in sodium reabsorption. Renal production of ammonium was not significantly different under basal conditions or 2 days after ischemia, but more ammonia was released by the urine in the postischemic dogs. Renal uptake of glutamine was similar in control and in postischemic kidneys. It is concluded that during the recovery phase of the ischemia, renal ammoniagenesis is conserved.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Renal Ammoniagenesis during the Recovery Phase of Postischemic Acute Renal Failure in the Dog1

Montañés¹,

Badia²,

Rengel³

et al. 1990

Kidney Blood Press Res

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“…The CRG after Unx has been widely studied in rodents where increased cell number and size and enhanced activity of the excretory structures occur [3][4][5]. Several in vivo studies have demonstrated that renal tissue undergoing CRG would be less susceptible to injury caused by induction of acute renal failure (ARF) [6][7][8][9][10][11]. Thus, in a rat model of glycerol-induced ARF, Ramos et al [6] determined that previous Unx enhanced the recovery of renal function, and suggested that hemodynamical changes during CRG, like an increase in RBF, accounted for the protection.…”

Section: Introductionmentioning

confidence: 99%

“…Several in vivo studies have demonstrated that renal tissue undergoing CRG would be less susceptible to injury caused by induction of acute renal failure (ARF) [6][7][8][9][10][11]. Thus, in a rat model of glycerol-induced ARF, Ramos et al [6] determined that previous Unx enhanced the recovery of renal function, and suggested that hemodynamical changes during CRG, like an increase in RBF, accounted for the protection. Induction of CRG also attenuated functional and histological damage after ischemia-induced ARF [7,8].…”

Section: Introductionmentioning

confidence: 99%

Compensatory renal growth protects mice against Shiga toxin 2-induced toxicity

et al. 2006

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Uninephrectomy (Unx) is followed by the compensatory renal growth (CRG) of the remaining kidney. Previous evidence has shown that during CRG, renal tissue is resistant to a variety of pathologies. We tested the hypothesis that the functional changes that take place during CRG could attenuate Shiga toxin (Stx) toxicity in a mouse model of Stx2-induced hemolytic uremic syndrome (HUS). The participation of nitric oxide (NO) was analyzed. After CRG induction with Unx, mice were exposed to a lethal dose of Stx2, and the degree of renal damage and mortality was measured. Stx2 effects on the growth, renal blood flow (RBF) and NO synthase (NOS) intrarenal expression in the remaining kidney were then studied. The induction of CRG strongly prevented Stx2-mediated mortality and renal damage. Administration of the NOS inhibitor NG-nitro-L-arginine methyl ester (L-NAME) during CRG partially impaired the protection. Both Stx2 and L-NAME interfered with the hypertrophic and hyperplastic responses to Unx, as well as with the increase in RBF. In intact mice, Stx2 decreased renal perfusion, inhibited endothelial NOS basal expression and enhanced inducible NOS expression; all of these effects were attenuated by prior Unx. It is concluded that during CRG mice are highly protected against Stx2 toxicity and lethality. The protective capacity of CRG could be related to the enhancement of renal perfusion and preservation of eNOS renal expression, counterbalancing two major pathogenic mechanisms of Stx2.

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“…On the other hand, UNX can also confer vascular protection in renal injury caused by Shiga toxin (3), glycerol (27), or acute ischemic renal failure (6). Thus a better understanding of the adaptive responses to UNX can unveil important protective mechanisms with clinical relevance.…”

mentioning

confidence: 99%

Nitric oxide in afferent arterioles after uninephrectomy depends on extracellularl-arginine

Helle

Skogstrand

Schwartz

et al. 2013

American Journal of Physiology-Renal Physiology

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Uninephrectomy (UNX) causes hyperperfusion of the contralateral remaining kidney via increased nitric oxide (NO) synthesis. Although the exact mechanism remains largely unknown, we hypothesize that this would be localized to the afferent arteriole and that it depends on cellular uptake of l-arginine. The experiments were performed in rats 2 days (early) or 6 wk (late) after UNX and compared with controls (Sham) to study acute and chronic effects on NO metabolism. Renal blood flow was increased after UNX (21 ± 2 ml·min(-1)·kg(-1) in sham, 30 ± 3 in early, and 26 ± 1 in late, P < 0.05). NO inhibition with N(ω)-nitro-L-arginine methyl ester hydrochloride (L-NAME) caused a greater increase in renal vascular resistance in early UNX compared with Sham and late UNX (138 ± 24 vs. 88 ± 10, and 84 ± 7%, P < 0.01). The lower limit of autoregulation was increased both in early and late UNX compared with Sham (P < 0.05). L-NAME did not affect the ANG II-induced contraction of isolated afferent arterioles (AA) from Sham. AA from early UNX displayed a more pronounced contraction in response to L-NAME (-57 ± 7 vs. -16 ± 7%, P < 0.05) and in the absence of L-arginine (-41 ± 4%, P < 0.05) compared with both late UNX and Sham. mRNA expression of endothelial NO synthase was reduced, whereas protein expression was unchanged. Cationic amino acid transporter-1 and -2 mRNA was increased, while protein was unaffected in isolated preglomerular resistance vessels. In conclusion, NO-dependent hyperperfusion of the remaining kidney in early UNX is associated with increased NO release from the afferent arteriole, which is highly dependent on extracellular L-arginine availability.

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Role of Hemodynamic Alterations in the Partial Protection Afforded by Uninephrectomy against Glycerol-Induced Acute Renal Failure in Rats

Cited by 13 publications

References 17 publications

Renal Ammoniagenesis during the Recovery Phase of Postischemic Acute Renal Failure in the Dog1

Renal Ammoniagenesis during the Recovery Phase of Postischemic Acute Renal Failure in the Dog1

Compensatory renal growth protects mice against Shiga toxin 2-induced toxicity

Nitric oxide in afferent arterioles after uninephrectomy depends on extracellularl-arginine

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