Taurine Modulates Arginine Vasopressin-Mediated Regulation of Renal Function

Mozaffari, Mahmood S.; Schaffer, David V.

doi:10.1097/00005344-200106000-00012

Cited by 24 publications

(28 citation statements)

References 25 publications

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“…In addition, taurine is known to be an important modulator and regulator of renal function, and it contributes to body-fluid and electrolyte homeostasis. This suggests a critical role for taurine in renal IR injury [ 27 , 28 ]. Like to taurine, the most important physiological roles for betaine are as an osmolyte and a methyl donor [ 29 ].…”

Section: Discussionmentioning

confidence: 99%

Proton Nuclear Magnetic Resonance (¹H-NMR)-Based Metabolomic Evaluation of Human Renal Allografts from Donations After Circulatory Death

et al. 2017

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Background:Delayed graft function (DGF) is a common complication that impairs allograft function after kidney transplantation. However, the mechanism of DGF remains unclear. Nuclear magnetic resonance (NMR)-based analysis has been widely used in recent times to assess changes in metabolite levels. Material/Methods:Samples of perfusate from allografts donated after circulatory death were collected prior to transplantation, during static cold storage.1 H-NMR-based metabolomics combined with the statistical methods, orthogonal partial least-squares discriminant analysis (OPLS-DA), and principle-component analysis (PCA), were employed to test different levels of metabolites between the allografts that exhibited DGF and those that exhibited immediate graft function (IGF). Results:The study population consisted of 36 subjects, 11 with DGF and 25 with IGF. Of the 37 detected and identified metabolites, a-glucose and citrate were significantly elevated in the perfusate of DGF allografts, and taurine and betaine were significantly decreased. Conclusions:1 H-NMR analysis of DGF and IGF perfusates revealed some significant differences in their metabolite profiles, which may help explain the mechanisms of kidney ischemia-reperfusion injury and DGF.

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Section: Discussionmentioning

confidence: 99%

Proton Nuclear Magnetic Resonance (¹H-NMR)-Based Metabolomic Evaluation of Human Renal Allografts from Donations After Circulatory Death

et al. 2017

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“…An increase of urea transport can be due to enhanced release of vasopressin which is known to stimulate urea transport [36]. In taurine-depleted rats, the plasma vasopressin level was significantly higher than in the control rats leading to the production of hyperosmolar urine [29]. Thus, increased vasopressin concentrations and stimulation of urea transport may maintain urinary concentrating ability despite the lack of one of the organic osmolytes.…”

Section: Discussionmentioning

confidence: 99%

Impaired ability to increase water excretion in mice lacking the taurine transporter gene TAUT

Huang

Boini

Lang

et al. 2005

Pflugers Arch - Eur J Physiol

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Cellular taurine uptake or release counteracts alterations of cell volume. Na+-coupled taurine transporter TAUT mediates concentrative cellular uptake of taurine. Inhibition of vasopressin secretion by hypotonicity may involve taurine release from glial cells of supraoptic nucleus. We compared renal function of mice lacking TAUT (taut-/-) and wild-type littermates (taut+/+). We observed renal taurine loss and subsequent hypotaurinemia in taut-/- mice. With free access to water, plasma and urine osmolality, urinary flow rate as well as urinary excretion and plasma concentrations of Na+ and K+ were similar in taut-/- and taut+/+ mice, whereas plasma concentrations of urea were enhanced in taut-/- mice. An oral water load (1 ml/16 g body weight) induced a similar diuresis in both genotypes. Repeating the oral water load immediately after normalization of urine flow rate, however, resulted in delayed diuresis and higher urinary vasopressin/creatinine ratios in taut-/- mice. In comparison, the repeated diuretic response to vasopressin V2 receptor blockade was not different between genotypes. Water deprivation for 36 h led to similar antidiuresis and increases of urinary osmolality in both genotypes. Upon free access to water after deprivation, taut-/- mice continued to concentrate urine up to 6 days, while taut+/+ mice rapidly returned to normal urinary osmolality. Urinary vasopressin/creatinine ratios and plasma aldosterone concentrations were not different under basal conditions but were significantly higher in taut-/- mice than in taut+/+ mice at 6 days after water deprivation. In conclusion, taut-/- mice suffer from renal taurine loss and impaired ability to lower urine osmolality and to increase urinary water excretion. The latter defect could reside extrarenally and result from a role of taurine in the suppression of vasopressin release which may be attenuated in taut-/- mice.

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“…; total of 90 minute post-infusion collection) were determined in pre-instrumented conscious animal. 3 H-Inulin was used for measurement of the glomerular filtration rate (GFR) [ 18 - 21 ].…”

Section: Methodsmentioning

confidence: 99%

“…These include its purported antioxidant, membrane stabilizing, cellular osmoregulatory and antiapoptotic effects [ 14 - 17 ]. In addition, we have shown that taurine is an important modulator/ regulator of renal function and therefore a contributor to body fluid and electrolyte homeostasis [ 18 - 21 ]. Thus we conjectured that body taurine status is an important determinant of the outcome of renal IR injury.…”

Section: Introductionmentioning

confidence: 99%

Differential effects of taurine treatment and taurine deficiency on the outcome of renal ischemia reperfusion injury

et al. 2010

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Taurine possesses membrane stabilization, osmoregulatory and antioxidant properties, aspects of relevance to ischemic injury. We tested the hypothesis that body taurine status is a determinant of renal ischemic injury. Accordingly, renal function and structure were examined in control (C), taurine-treated (TT) and taurine deficient (TD) rats that were subjected to bilateral renal ischemia (60 min) followed by reperfusion (IR); sham operated rats served as controls. Baseline urine osmolality was greater in the TD group than in the control and the TT groups, an effect associated with increased renal aquaporin 2 level. The IR insult reduced urine osmolality (i.e., day-1 post insult); the TD/IR group displayed a more marked recovery in urine osmolality by day-6 post insult than the other two groups. Fluid and sodium excretions were lower in the TD/IR group, suggesting propensity to retention. Histopathological examination revealed the presence of tubular necrotic foci in the C/IR group than sham controls. While renal architecture of the TD/IR group showed features resembling sham controls, the TT/IR group showed dilated tubules, which lacked immunostaining for aquaporin 2, but not 1, suggestive of proximal tubule origin. Finally, assessment of cell proliferation and apoptosis revealed lower proliferation but higher apoptotic foci in the TT/IR group than other IR groups. Collectively, the results indicate that body taurine status is a major determinant of renal IR injury.

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Taurine Modulates Arginine Vasopressin-Mediated Regulation of Renal Function

Cited by 24 publications

References 25 publications

Proton Nuclear Magnetic Resonance (¹H-NMR)-Based Metabolomic Evaluation of Human Renal Allografts from Donations After Circulatory Death

Proton Nuclear Magnetic Resonance (¹H-NMR)-Based Metabolomic Evaluation of Human Renal Allografts from Donations After Circulatory Death

Impaired ability to increase water excretion in mice lacking the taurine transporter gene TAUT

Differential effects of taurine treatment and taurine deficiency on the outcome of renal ischemia reperfusion injury

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