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R M Huisman - One of the best experts on this subject based on the ideXlab platform.

  • Renal 131I-Hippurate clearance overestimates true renal blood flow in the instrumented conscious dog.
    The American journal of physiology, 1996
    Co-Authors: C A Visscher, P E De Jong, D De Zeeuw, G Navis, A K Van Zanten, R M Huisman
    Abstract:

    We evaluated renal 131I-Hippurate clearance (ERPFhip) as a measure of renal blood flow (RBF) in chronically instrumented conscious dogs. When adjusted for renal Hippurate extraction (Ehip, 0.77 +/- 0.01) and hematocrit (Hct, 39.7 +/- 1%), calculated RBFhip (656 +/- 37 ml/min) markedly exceeded renal blood flow measured with renal artery blood flow probes (RBFprobe, 433 +/- 27 ml/min). The discrepancy could not be explained by flow probe calibration, because in vivo comparison of flow probe values with renal venous outflow showed only a slight underestimation of renal blood flow (slope 0.93, 95% confidence interval 0.89-0.97). Redistribution of Hippurate from erythrocytes into renal venous plasma during or shortly after blood sampling led to an underestimation of Ehip by 4 +/- 1% and thus could only explain a small part of the difference. Extrarenal Hippurate clearance was excluded, because the amount of 131I-Hippurate cleared from plasma equaled that appearing in the urine (303 +/- 17 and 307 +/- 17 ml/min). Applying these corrections, we found that RBFhip still exceeded RBFprobe by 37 +/- 3%. These data indicate that renal blood flow measured by the Hippurate clearance technique markedly overestimates true renal blood flow. Because other errors were excluded, a combination of sampling of nonrenal blood and intrarenal Hippurate extraction from erythrocytes might play a role.

  • angiotensin converting enzyme inhibition induced changes in Hippurate renography and renal function in renovascular hypertension
    The Journal of Nuclear Medicine, 1996
    Co-Authors: C A Visscher, Dick De Zeeuw, P E De Jong, Da Piers, H Beekhuis, G M M Groothuis, R M Huisman
    Abstract:

    We studied the mechanism of angiotensin-converting enzyme (ACE) inhibition-induced changes in Hippurate renography of the poststenotic kidney. Methods: Ten male mongrel dogs, six with unilateral and four with bilateral renal artery stenosis, were equipped with renal artery blood flow probes and catheters in the aorta, atrium and both renal veins. Results: Enalaprilat (10 mg intravenously) in conscious dogs with renal artery stenoses produced changes in ail stenotic (n = 11) but not in nonstenotic kidney I-123-Hippurate renograms (n = 6), Renographic changes correlated significantly with initiation of intrarenal I-131-Hippurate retention, a decrease in mean arterial pressure (MAP), renal extraction of I-131-Hippurate and I-125-iothalamate (r = 0.68, r = 0.62, r = 0.84, r = 0.83, respectively) but not with renal blood flow changes (r = 0.34), Furthermore, renal uptake of I-131-Hippurate and I-125-iothalamate decreased in stenotic kidneys with a grade II renogram (-52 +/- 11% and -79 +/- 6%, respectively), Iodine-125-Hippurate autoradiograms of stenotic kidneys during ACE inhibition showed tracer retention mainly in the proximal tubular cells. Results during osmotic diuresis supported our findings. Conclusion: Angiotensin-converting enzyme inhibition-induced Hippurate retention curves of poststenotic kidneys appear to result from a sequence of events, A decrease in MAP combined with efferent vasodilation leads to a decrease in intraglomerular capillary pressure. This decrease in pressure causes a decease in glomerular filtration rate and proximal tubular urine flow, This decrease in turn hampers tubular Hippurate transit and transport across the luminal membrane, leading to intrarenal Hippurate retention and, in more severe cases, decreased renal Hippurate uptake.

  • drug induced changes in renal Hippurate clearance as a measure of renal blood flow
    Kidney International, 1995
    Co-Authors: Antoinette C Visscher, Dick De Zeeuw, Paul E De Jong, Wim J Sluiter, R M Huisman
    Abstract:

    Drug-induced changes in renal Hippurate clearance as a measure of renal blood flow. We studied the accuracy of the plasma 131 I-Hippurate clearance technique to monitor drug-induced changes in renal blood flow (RBF) by comparing it to a flow probe technique in six conscious, chronically instrumented dogs. Placebo caused no change in RBF, either established by Hippurate clearance (ERPF hip ) or by renal blood flow probe (RBF probe ). Enalaprilate induced a rise in ERPF hip and RBF probe (+26 ± 5 and 44 ± 12%), as did dopamine (+16 ± 4 and +33 ± 5%). Intravenous infusion of norepinephrine induced a rise in ERPF hip (+2 ± 6%, NS) and in RBFprobe (+18 ± 3%), as did nitroprusside (+14 ± 4% and +13 ± 6%, NS). Indomethacin induced a fall in ERPF hip (-8 ± 2%) and in RBF probe (-7 ± 3%, NS), as did angiotensin II (-19 ± 1 and -26 ± 3%). Renal Hippurate extraction (E hip ) was affected by enalaprilate, dopamine, and angiotensin II (-5 ±2, -7 ± 1, and +5 ± 2%, respectively). Hematocrit (Hct) was affected by dopamine, norepinephrine, and nitroprusside (+2 ± 1, +6 ± 1, and - 6 ± 2%, respectively). Drug-induced changes in ERPF hip correlated well with changes in RBF probe (r = 0.902, P hip did not independently affect this relation, whereas changes in Hct did: ΔRBF(% of baseline) = 1.529 × ΔERPF hip (% of baseline) + 1.296 × ΔHct(% of baseline). These data indicate that drug-induced changes in plasma Hippurate clearance can, even when changes in renal Hippurate extraction are unknown, be used as a reliable indicator of changes in renal blood flow if changes in hematocrit are taken into account.

Stig Nilsson - One of the best experts on this subject based on the ideXlab platform.

  • long term treatment with methenamine Hippurate in recurrent urinary tract infection
    Acta Medica Scandinavica, 2009
    Co-Authors: Stig Nilsson
    Abstract:

    Abstract. Twenty-four patients with a history of recurrent urinary tract infection and in whom residual urine was considered to be a factor of importance for chronicity, have been treated for an average of 16 months with 1 g methenamine Hippurate morning and evening. No patient had urinary calculus at the commencement of treatment and neither did any patient have an indwelling catheter. In patients without urinary tract infection or in whom abacteriuria was achieved with methenamine Hippurate, the number of reinfections was reduced by approximately two thirds compared to periods prior to treatment. No patient was completely free from infection throughout the whole treatment period. However, in no case did bacteria with extensive resistance appear. When urinary tract infection was treated with methenamine Hippurate, abacteriuria was achieved in only 6 of 14 patients. It would therefore seem that this agent is only of limited value for treatment of established infection. In the event of manifest infection it would appear appropriate to treat the infection primarily with antibiotics and to use methenamine Hippurate for prophylaxis when abacteriuria has been achieved. No patient developed urinary calculus during treatment with methenamine Hippurate and no deterioration of renal function or haematological change was observed.

Muhammad Nazrul Hakim - One of the best experts on this subject based on the ideXlab platform.

  • Preparation of Hippurate-zinc layered hydroxide nanohybrid and its synergistic effect with tamoxifen on HepG2 cell lines
    International Journal of Nanomedicine, 2011
    Co-Authors: Mothanna Al-qubaisi, Mohd Zobir Hussein, Zulkarnain Zainal, Muhammad Nazrul Hakim
    Abstract:

    Background A new simple preparation method for a Hippurate-intercalated zinc-layered hydroxide (ZLH) nanohybrid has been established, which does not need an anion-exchange procedure to intercalate the Hippurate anion into ZLH interlayers.

  • preparation of Hippurate zinc layered hydroxide nanohybrid and its synergistic effect with tamoxifen on hepg2 cell lines
    International Journal of Nanomedicine, 2011
    Co-Authors: Mothanna Alqubaisi, Mohd Zobir Hussein, Zulkarnain Zainal, Muhammad Nazrul Hakim
    Abstract:

    BACKGROUND: A new simple preparation method for a Hippurate-intercalated zinc-layered hydroxide (ZLH) nanohybrid has been established, which does not need an anion-exchange procedure to intercalate the Hippurate anion into ZLH interlayers. METHODS: The hippuric acid nanohybrid (HAN) was prepared by direct reaction of an aqueous suspension of zinc oxide with a solution of hippuric acid via a one-step method. RESULTS: The basal spacing of the nanohybrid was 21.3 A, indicating that the Hippurate anion was successfully intercalated into the interlayer space of ZLH, and arranged in a monolayer fashion with the carboxylate group pointing toward the ZLH inorganic interlayers. A Fourier transform infrared study confirmed the formation of the nanohybrid, while thermogravimetry and differential thermogravimetry analyses showed that the thermal stability of the nanohybrid was markedly enhanced. The loading of Hippurate in the nanohybrid was estimated to be about 38.7% (w/w), and the release of Hippurate from the nanohybrid was of a controlled manner, and therefore the resulting material was suitable for use as a controlled-release formulation. HAN has synergistic properties with tamoxifen toward a HepG2 cell line, with an IC50 value of 0.35 compared with Hippurate. In the antiproliferative assay, the ratio of viable cells account for cells treated by the combination tamoxifen with HAN to untreated cells was sharply reduced from 66% to 13% after 24 and 72 hours, respectively. CONCLUSION: The release of hippuric acid anions from HAN occurred in a controlled manner, and the resulting material is suitable for a controlled-release formulation.

Rastislav Dzúrik - One of the best experts on this subject based on the ideXlab platform.

  • Hippurate participates in the correction of metabolic acidosis
    Kidney International, 2001
    Co-Authors: Rastislav Dzúrik, Viera Spustová, Zora Krivošíková, K Gazdikova
    Abstract:

    Hippurate participates in the correction of metabolic acidosis. Hippurate (Hip), an endogenous conjugate, belongs to the group of uremic toxins. Hip stimulates P-independent glutaminase (PIG) localized at the proximal luminal membrane, desamidating glutamine with the formation of ammonia, a dominant and adaptive elimination product of H+. This appears to be important because metabolic acidosis (MAC) does not stimulate PIG. Moreover, Hip inhibits ammonia production by P-dependent mitochondrial glutaminase (PDG) that is primarily stimulated by MAC. By this mechanism, it shifts the ammonia production from mitochondria to proximal tubular lumen. MAC stimulates Hip synthesis in the liver and kidney and increases Hip plasma concentration and even fractional excretion by the kidney, which creates an effective regulatory loop of ammoniagenesis. Thus, it appears that Hip by its participation in the correction of MAC possesses the modulatory function.

  • Participation of P-dependent and P-independent glutaminases in rat kidney ammoniagenesis and their modulation by metabolic acidosis, Hippurate and insulin.
    Physiological Research, 1998
    Co-Authors: Zora Krivošíková, Spustová, Rastislav Dzúrik
    Abstract:

    The key regulatory enzymes of kidney ammoniagenesis appear to be P-dependent (PDG) and P-independent (PIG) glutaminases. While the participation of PDG has been satisfactorily elucidated, the significance of PIG remains doubtful. Rat kidney cortex slices synthesized ammonia even under basal conditions. Metabolic acidosis, Hippurate and insulin stimulated ammonia production. Under basal conditions, PDG activity in kidney homogenate, was twice as high as PIG activity. Metabolic acidosis stimulated ammonia production by the stimulation of both PDG (100%) and PIG (57%) activities. Hippurate stimulated only PIG activity both under basal conditions (90%) and in metabolic acidosis (52%), while it inhibited PDG activity only insignificantly under basal conditions and markedly (53%) in metabolic acidosis. Insulin stimulated both PIG and PDG activities under basal conditions as well as in metabolic acidosis and potentiated the PIG stimulation by Hippurate while it potentiated the Hippurate inhibition of PDG both under basal conditions and in acidotic rats. In conclusion, both PDG and PIG participate in ammoniagenesis and are stimulated by metabolic acidosis and insulin. Hippurate stimulates PIG, while it inhibits PDG in metabolic acidosis and even after insulin administration. The effect of Hippurate appears to be of physiological interest.

  • The effect of dipyridamole on Hippurate excretion in healthy volunteers and in patients with renal insufficiency
    Casopís lékar̆ů c̆eských, 1991
    Co-Authors: Gajdos M, Stefíková K, Spustová, Rastislav Dzúrik
    Abstract:

    Organic anions retained in patients with renal failure participate in a substantial way in the metabolic acidosis and thus also the catabolism in renal failure. The basic disorder is the reduced capacity of the transport system of organic ions. Therefore drugs are sought to enhance its activity. Acute investigation of healthy volunteers revealed that 150 mg dipyridamol increased the urinary Hippurate excretion, while the serum Hippurate concentration declined. In patients with renal failure there is the same tendency, though less marked, and due to the variability of functions of individual patients this trend is insignificant. It is assumed that this hitherto not described action of dipyridamol may be of therapeutic importance when administered to patients with impaired renal function.

  • Effect of Hippurate on Glucose Utilization in Rat Kidney Cortex Slices
    Kidney & Blood Pressure Research, 1991
    Co-Authors: Viera Spustová, Rastislav Dzúrik
    Abstract:

    Hippurate action on glucose utilization was evaluated in rat kidney cortex slices. Studies have shown the following. (1) Hippurate inhibits markedly basal as well as insulin-stimulated glucose utiliza

  • Effect of Hippurate on glucose utilization in rat kidney cortex slices.
    Renal physiology and biochemistry, 1991
    Co-Authors: Viera Spustová, Rastislav Dzúrik
    Abstract:

    Hippurate action on glucose utilization was evaluated in rat kidney cortex slices. Studies have shown the following. (1) Hippurate inhibits markedly basal as well as insulin-stimulated glucose utilization and basal gluconeogenesis. (2) Ca deficiency and specific Ca channel blockers diltiazem and isradipine abolish the Hippurate inhibition of glucose utilization. (3) K+ channel blockers, i.e. the increased K+ concentration in incubation medium, procaine and sulfonylurea drugs also abolish the Hippurate inhibition of glucose utilization. It is concluded that Hippurate and benzoate operate through the ATP-dependent K+ channel.

Dennis M Bier - One of the best experts on this subject based on the ideXlab platform.

  • comparison of serine and Hippurate as precursor equivalents during infusion of 15n glycine for measurement of fractional synthetic rates of apolipoprotein b of very low density lipoprotein
    Metabolism-clinical and Experimental, 1995
    Co-Authors: Jann Arends, Dennis M Bier, Gertrud Schafer, Peter Schauder, Johannes Bircher
    Abstract:

    Abstract Enrichment in Hippurate has been measured to indicate precursor enrichment during glycine tracer infusion studies to estimate fractional synthetic rates of individual hepatic export proteins. However, Hippurate tends to overestimate precursor enrichment. Since glycine is rapidly converted to serine by liver cells, we compared tracer enrichment in Hippurate and serine with that of glycine incorporated into apolipoprotein (apo) B-100. Ten healthy control subjects were studied in the postabsorptive state during an 8-hour primed-constant infusion of [ 15 N ]glycine (10 μmol · kg −1 · h −1 ). Apo B of very-low-density lipoprotein (VLDL) was isolated by standard ultracentrifugation and isopropanol precipitation. Glycine and serine were isolated from plasma and hydrolyzed apo B, Hippurate was isolated from plasma, and [ 15 N ]enrichment was determined by gas chromatography-mass spectrometry. Enrichment in serine and glycine isolated from apo B was identical at all time points, and their enrichment in apo B increased asymptotically, approaching an apparent plateau (mean ± SD: 91% ± 10% of calculated plateau at 8 hours) that was taken to represent hepatic protein precursor enrichment. Enrichment in both plasma serine and Hippurate followed a biphasic pattern and continued to increase until the end of the study, raising the possibility that precursor enrichment had not reached a steady state during the study. The apo B plateau was lower (factor 0.76 ± 0.27) than the final enrichment in Hippurate and higher (factor 1.38 ± 0.36) than that in plasma serine; however, predictions of protein precursor enrichment based on either metabolite were flawed by a large coefficient of variation (35% v 26%). We conclude that glycine enrichment in the hepatic protein precursor pool may not be constant during an 8-hour infusion study, and that only a rough approximation of this level may be obtained using either enrichment in plasma Hippurate or plasma serine.

  • analysis of plasma Hippurate in humans using gas chromatography mass spectrometry concentration and incorporation of infused 15n glycine
    Analytical Biochemistry, 1990
    Co-Authors: Jann Arends, Francis Chiu, Dennis M Bier
    Abstract:

    Abstract To allow in vivo determination of synthetic rates for individual proteins, physiological incorporation of infused [15N]glycine into urinary hippuric acid has been used as an indicator of intrahepatic tracer dilution. Although the kidneys might contribute to Hippurate production, the relationship between hepatic, plasma, and urinary Hippurate has not yet been established in humans. To further investigate these issues we developed a fast, sensitive, and reliable method for measuring simultaneously Hippurate concentrations and in vivo tracer incorporation into Hippurate in plasma and urine using stable isotopes and gas chromatography-mass spectrometry. We then tested this assay under several experimental conditions. Reference compounds ([15N]-and [ring-2H5]Hippurate) were synthesized and gave linear standard curves. Postabsorptive Hippurate plasma levels in healthy subjects ranged from 1.2 to 10.5 μ m and protein binding was 79 ± 6% (mean ± SD). Following a bolus dose of [15N]glycine tracer appeared in plasma Hippurate; enrichment in Hippurate was indistinguishable from that in glycine after an equilibration period of 20 min, indicating a close relationship between intracellular glycine and plasma Hippurate. A 16-h infusion of [15N]glycine resulted in identical enrichment levels in urinary and plasma Hippurate; glycine enrichment in a hepatic export protein (VLDL-ApoB) was approaching plasma Hippurate but not plasma free glycine enrichment. The ability to monitor plasma Hippurate is of practical advantage compared to the sampling of urine. Furthermore it allows the monitoring of rapid events in the intrahepatic dilution of an infused glycine tracer. This assay may, therefore, become an important tool in the study of hepatic protein metabolism.