Urinary Excretion

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Tetsuya Yamamoto - One of the best experts on this subject based on the ideXlab platform.

  • Effects of sucrose on plasma concentrations and Urinary Excretion of purine bases.
    Metabolism, 2007
    Co-Authors: Terumi Kobayashi, Taku Inokuchi, Asako Yamamoto, Sumio Takahashi, Zenta Tsutsumi, Hiroki Saito, Yuji Moriwaki, Tetsuya Yamamoto
    Abstract:

    To determine whether an increase in the plasma concentration of uric acid by sucrose intake is ascribable to enhanced purine degradation and/or decreased Urinary Excretion of uric acid, we measured the plasma concentrations of purine bases (uric acid, hypoxanthine, and xanthine) and uridine, as well as the Urinary Excretion of purine bases in 7 healthy subjects before and after administering sucrose at 1.5 g/kg of body weight in 2 related experiments, with and without an administration of 300 mg of allopurinol. In addition, in the control experiment without an administration of sugar and with an administration of 300 mg of allopurinol, we measured the same parameters in those 7 subjects. Without added allopurinol, sucrose increased the plasma concentration of uric acid by 11% (P < .01) as well as that of uridine, although it did not significantly increase the plasma concentrations of hypoxanthine and xanthine or the Urinary Excretion of uric acid. On the other hand, the plasma concentration and Urinary Excretion of hypoxanthine were increased by 2.4-fold (P < .05) and 3.42-fold (P < .05), respectively, and the plasma concentration of xanthine was increased by 1.2-fold (P < .05) together with an increase in the plasma concentration of uridine in the experiment with allopurinol administration. In contrast, the plasma concentration and Urinary Excretion of uric acid and the Urinary Excretion of xanthine were not increased. In addition, in the control experiment, all parameters did not change significantly. These results indicate that purine degradation enhanced by sucrose plays a major role in the increased plasma concentration of uric acid.

  • Effect of octreotide acetate on the plasma concentration and Urinary Excretion of uridine and purine bases.
    Endocrine Journal, 2002
    Co-Authors: Tetsuya Yamamoto, Sumio Takahashi, Zenta Tsutsumi, Yuji Moriwaki, Toshikazu Hada
    Abstract:

    To determine the effect of octreotide acetate on Urinary Excretion of uric acid and plasma concentration of uridine, we subcutaneously administered octreotide acetate (1 microg/kg of body weight) to 5 healthy subjects. Ninety minutes after administration, octreotide acetate increased the plasma concentration of uridine by 15% and decreased the plasma concentration of glucagon by 24% and that of insulin to below the detection limits. In addition, octreotide acetate decreased the Urinary Excretion of uric acid, sodium, and chloride by 60%, 40%, and 38%, respectively, at 1 hour after administration. However, octreotide acetate did not affect the concentrations of hypoxanthine, xanthine, uric acid, cyclic AMP in plasma, lactic acid and pyruvic acid in blood, Urinary Excretion of hypoxanthine and xanthine, or creatinine clearance. From these results, we speculated that octreotide acetate decreases the Urinary Excretion of uric acid by decreasing the concentration of glucagon and/or Urinary Excretion of sodium, and increases the plasma concentration of uridine via decreased concentrations of glucagon and insulin.

  • Effect of norepinephrine on the Urinary Excretion of purine bases and oxypurinol
    Metabolism, 2001
    Co-Authors: Tetsuya Yamamoto, Sumio Takahashi, Zenta Tsutsumi, Yuji Moriwaki, Toshikazu Hada
    Abstract:

    To examine whether norepinephrine affects the plasma concentrations and Urinary Excretion of purine bases and oxypurinol, we orally administered allopurinol (300 mg) to 5 healthy subjects and 9 hours later intravenously administered norepinephrine (12 to 20 [mu ]g/kg body weight), which causes a more than 10 mm Hg increase in diastolic pressure for 2 hours. Norepinephrine decreased the Urinary Excretion of uric acid by 33% (P [lt ] .01), oxypurinol by 32% (P [lt ] .01), and xanthine by 51% (P [lt ] .01), as well as the fractional clearance of uric acid by 32% (P [lt ] .01), oxypurinol by 24% (P [lt ] .05), and xanthine by 21% (P [lt ] .05) when measured 1 to 2 hours after administration. These results indicate that norepinephrine decreases the Urinary Excretion of uric acid, oxypurinol, and xanthine, probably via hemodynamic change. It is also suggested that the hypouricemic effect of allopurinol may be more potent than that expected in gout patients with enhanced sympathetic tone, such as in salt-sensitive hypertension.

  • Effects of fructose and xylitol on the Urinary Excretion of adenosine, uridine, and purine bases.
    Metabolism, 1999
    Co-Authors: Tetsuya Yamamoto, Sumio Takahashi, Zenta Tsutsumi, Yuji Moriwaki, Jun-ichi Yamakita, Kazuya Higashino
    Abstract:

    To examine whether fructose and xylitol increase the plasma concentration and Urinary Excretion of adenosine, as well as uridine and purine bases (hypoxanthine, xanthine, and uric acid), we intravenously administered xylitol and, 2 weeks later, fructose, to five healthy subjects. Analyses of blood and urine samples obtained during these infusion studies demonstrated that fructose increased the Urinary Excretion of adenosine and uridine 11.9- and 105.5-fold, respectively, and caused only a small increase in the plasma concentrations of uridine and purine bases. It was further demonstrated that xylitol increased the Urinary Excretion of uridine 58.4-fold, with a marked increase in the plasma concentrations of purine bases and uridine but without an increase in the Urinary Excretion of adenosine. However, neither infusion increased the plasma concentration of adenosine. These results suggest that in addition to many organs, including the liver, fructose is significantly metabolized by an abrupt adenosine triphosphate (ATP) consumption in the kidney, leading to an increase in the Urinary Excretion of adenosine and uridine. They also suggest that xylitol is not significantly metabolized in the kidney.

Zenta Tsutsumi - One of the best experts on this subject based on the ideXlab platform.

  • Effects of sucrose on plasma concentrations and Urinary Excretion of purine bases.
    Metabolism, 2007
    Co-Authors: Terumi Kobayashi, Taku Inokuchi, Asako Yamamoto, Sumio Takahashi, Zenta Tsutsumi, Hiroki Saito, Yuji Moriwaki, Tetsuya Yamamoto
    Abstract:

    To determine whether an increase in the plasma concentration of uric acid by sucrose intake is ascribable to enhanced purine degradation and/or decreased Urinary Excretion of uric acid, we measured the plasma concentrations of purine bases (uric acid, hypoxanthine, and xanthine) and uridine, as well as the Urinary Excretion of purine bases in 7 healthy subjects before and after administering sucrose at 1.5 g/kg of body weight in 2 related experiments, with and without an administration of 300 mg of allopurinol. In addition, in the control experiment without an administration of sugar and with an administration of 300 mg of allopurinol, we measured the same parameters in those 7 subjects. Without added allopurinol, sucrose increased the plasma concentration of uric acid by 11% (P < .01) as well as that of uridine, although it did not significantly increase the plasma concentrations of hypoxanthine and xanthine or the Urinary Excretion of uric acid. On the other hand, the plasma concentration and Urinary Excretion of hypoxanthine were increased by 2.4-fold (P < .05) and 3.42-fold (P < .05), respectively, and the plasma concentration of xanthine was increased by 1.2-fold (P < .05) together with an increase in the plasma concentration of uridine in the experiment with allopurinol administration. In contrast, the plasma concentration and Urinary Excretion of uric acid and the Urinary Excretion of xanthine were not increased. In addition, in the control experiment, all parameters did not change significantly. These results indicate that purine degradation enhanced by sucrose plays a major role in the increased plasma concentration of uric acid.

  • Effect of octreotide acetate on the plasma concentration and Urinary Excretion of uridine and purine bases.
    Endocrine Journal, 2002
    Co-Authors: Tetsuya Yamamoto, Sumio Takahashi, Zenta Tsutsumi, Yuji Moriwaki, Toshikazu Hada
    Abstract:

    To determine the effect of octreotide acetate on Urinary Excretion of uric acid and plasma concentration of uridine, we subcutaneously administered octreotide acetate (1 microg/kg of body weight) to 5 healthy subjects. Ninety minutes after administration, octreotide acetate increased the plasma concentration of uridine by 15% and decreased the plasma concentration of glucagon by 24% and that of insulin to below the detection limits. In addition, octreotide acetate decreased the Urinary Excretion of uric acid, sodium, and chloride by 60%, 40%, and 38%, respectively, at 1 hour after administration. However, octreotide acetate did not affect the concentrations of hypoxanthine, xanthine, uric acid, cyclic AMP in plasma, lactic acid and pyruvic acid in blood, Urinary Excretion of hypoxanthine and xanthine, or creatinine clearance. From these results, we speculated that octreotide acetate decreases the Urinary Excretion of uric acid by decreasing the concentration of glucagon and/or Urinary Excretion of sodium, and increases the plasma concentration of uridine via decreased concentrations of glucagon and insulin.

  • Effect of norepinephrine on the Urinary Excretion of purine bases and oxypurinol
    Metabolism, 2001
    Co-Authors: Tetsuya Yamamoto, Sumio Takahashi, Zenta Tsutsumi, Yuji Moriwaki, Toshikazu Hada
    Abstract:

    To examine whether norepinephrine affects the plasma concentrations and Urinary Excretion of purine bases and oxypurinol, we orally administered allopurinol (300 mg) to 5 healthy subjects and 9 hours later intravenously administered norepinephrine (12 to 20 [mu ]g/kg body weight), which causes a more than 10 mm Hg increase in diastolic pressure for 2 hours. Norepinephrine decreased the Urinary Excretion of uric acid by 33% (P [lt ] .01), oxypurinol by 32% (P [lt ] .01), and xanthine by 51% (P [lt ] .01), as well as the fractional clearance of uric acid by 32% (P [lt ] .01), oxypurinol by 24% (P [lt ] .05), and xanthine by 21% (P [lt ] .05) when measured 1 to 2 hours after administration. These results indicate that norepinephrine decreases the Urinary Excretion of uric acid, oxypurinol, and xanthine, probably via hemodynamic change. It is also suggested that the hypouricemic effect of allopurinol may be more potent than that expected in gout patients with enhanced sympathetic tone, such as in salt-sensitive hypertension.

  • Effects of fructose and xylitol on the Urinary Excretion of adenosine, uridine, and purine bases.
    Metabolism, 1999
    Co-Authors: Tetsuya Yamamoto, Sumio Takahashi, Zenta Tsutsumi, Yuji Moriwaki, Jun-ichi Yamakita, Kazuya Higashino
    Abstract:

    To examine whether fructose and xylitol increase the plasma concentration and Urinary Excretion of adenosine, as well as uridine and purine bases (hypoxanthine, xanthine, and uric acid), we intravenously administered xylitol and, 2 weeks later, fructose, to five healthy subjects. Analyses of blood and urine samples obtained during these infusion studies demonstrated that fructose increased the Urinary Excretion of adenosine and uridine 11.9- and 105.5-fold, respectively, and caused only a small increase in the plasma concentrations of uridine and purine bases. It was further demonstrated that xylitol increased the Urinary Excretion of uridine 58.4-fold, with a marked increase in the plasma concentrations of purine bases and uridine but without an increase in the Urinary Excretion of adenosine. However, neither infusion increased the plasma concentration of adenosine. These results suggest that in addition to many organs, including the liver, fructose is significantly metabolized by an abrupt adenosine triphosphate (ATP) consumption in the kidney, leading to an increase in the Urinary Excretion of adenosine and uridine. They also suggest that xylitol is not significantly metabolized in the kidney.

Yuji Moriwaki - One of the best experts on this subject based on the ideXlab platform.

  • Effects of sucrose on plasma concentrations and Urinary Excretion of purine bases.
    Metabolism, 2007
    Co-Authors: Terumi Kobayashi, Taku Inokuchi, Asako Yamamoto, Sumio Takahashi, Zenta Tsutsumi, Hiroki Saito, Yuji Moriwaki, Tetsuya Yamamoto
    Abstract:

    To determine whether an increase in the plasma concentration of uric acid by sucrose intake is ascribable to enhanced purine degradation and/or decreased Urinary Excretion of uric acid, we measured the plasma concentrations of purine bases (uric acid, hypoxanthine, and xanthine) and uridine, as well as the Urinary Excretion of purine bases in 7 healthy subjects before and after administering sucrose at 1.5 g/kg of body weight in 2 related experiments, with and without an administration of 300 mg of allopurinol. In addition, in the control experiment without an administration of sugar and with an administration of 300 mg of allopurinol, we measured the same parameters in those 7 subjects. Without added allopurinol, sucrose increased the plasma concentration of uric acid by 11% (P < .01) as well as that of uridine, although it did not significantly increase the plasma concentrations of hypoxanthine and xanthine or the Urinary Excretion of uric acid. On the other hand, the plasma concentration and Urinary Excretion of hypoxanthine were increased by 2.4-fold (P < .05) and 3.42-fold (P < .05), respectively, and the plasma concentration of xanthine was increased by 1.2-fold (P < .05) together with an increase in the plasma concentration of uridine in the experiment with allopurinol administration. In contrast, the plasma concentration and Urinary Excretion of uric acid and the Urinary Excretion of xanthine were not increased. In addition, in the control experiment, all parameters did not change significantly. These results indicate that purine degradation enhanced by sucrose plays a major role in the increased plasma concentration of uric acid.

  • Effect of octreotide acetate on the plasma concentration and Urinary Excretion of uridine and purine bases.
    Endocrine Journal, 2002
    Co-Authors: Tetsuya Yamamoto, Sumio Takahashi, Zenta Tsutsumi, Yuji Moriwaki, Toshikazu Hada
    Abstract:

    To determine the effect of octreotide acetate on Urinary Excretion of uric acid and plasma concentration of uridine, we subcutaneously administered octreotide acetate (1 microg/kg of body weight) to 5 healthy subjects. Ninety minutes after administration, octreotide acetate increased the plasma concentration of uridine by 15% and decreased the plasma concentration of glucagon by 24% and that of insulin to below the detection limits. In addition, octreotide acetate decreased the Urinary Excretion of uric acid, sodium, and chloride by 60%, 40%, and 38%, respectively, at 1 hour after administration. However, octreotide acetate did not affect the concentrations of hypoxanthine, xanthine, uric acid, cyclic AMP in plasma, lactic acid and pyruvic acid in blood, Urinary Excretion of hypoxanthine and xanthine, or creatinine clearance. From these results, we speculated that octreotide acetate decreases the Urinary Excretion of uric acid by decreasing the concentration of glucagon and/or Urinary Excretion of sodium, and increases the plasma concentration of uridine via decreased concentrations of glucagon and insulin.

  • Effect of norepinephrine on the Urinary Excretion of purine bases and oxypurinol
    Metabolism, 2001
    Co-Authors: Tetsuya Yamamoto, Sumio Takahashi, Zenta Tsutsumi, Yuji Moriwaki, Toshikazu Hada
    Abstract:

    To examine whether norepinephrine affects the plasma concentrations and Urinary Excretion of purine bases and oxypurinol, we orally administered allopurinol (300 mg) to 5 healthy subjects and 9 hours later intravenously administered norepinephrine (12 to 20 [mu ]g/kg body weight), which causes a more than 10 mm Hg increase in diastolic pressure for 2 hours. Norepinephrine decreased the Urinary Excretion of uric acid by 33% (P [lt ] .01), oxypurinol by 32% (P [lt ] .01), and xanthine by 51% (P [lt ] .01), as well as the fractional clearance of uric acid by 32% (P [lt ] .01), oxypurinol by 24% (P [lt ] .05), and xanthine by 21% (P [lt ] .05) when measured 1 to 2 hours after administration. These results indicate that norepinephrine decreases the Urinary Excretion of uric acid, oxypurinol, and xanthine, probably via hemodynamic change. It is also suggested that the hypouricemic effect of allopurinol may be more potent than that expected in gout patients with enhanced sympathetic tone, such as in salt-sensitive hypertension.

  • Effects of fructose and xylitol on the Urinary Excretion of adenosine, uridine, and purine bases.
    Metabolism, 1999
    Co-Authors: Tetsuya Yamamoto, Sumio Takahashi, Zenta Tsutsumi, Yuji Moriwaki, Jun-ichi Yamakita, Kazuya Higashino
    Abstract:

    To examine whether fructose and xylitol increase the plasma concentration and Urinary Excretion of adenosine, as well as uridine and purine bases (hypoxanthine, xanthine, and uric acid), we intravenously administered xylitol and, 2 weeks later, fructose, to five healthy subjects. Analyses of blood and urine samples obtained during these infusion studies demonstrated that fructose increased the Urinary Excretion of adenosine and uridine 11.9- and 105.5-fold, respectively, and caused only a small increase in the plasma concentrations of uridine and purine bases. It was further demonstrated that xylitol increased the Urinary Excretion of uridine 58.4-fold, with a marked increase in the plasma concentrations of purine bases and uridine but without an increase in the Urinary Excretion of adenosine. However, neither infusion increased the plasma concentration of adenosine. These results suggest that in addition to many organs, including the liver, fructose is significantly metabolized by an abrupt adenosine triphosphate (ATP) consumption in the kidney, leading to an increase in the Urinary Excretion of adenosine and uridine. They also suggest that xylitol is not significantly metabolized in the kidney.

Sumio Takahashi - One of the best experts on this subject based on the ideXlab platform.

  • Effects of sucrose on plasma concentrations and Urinary Excretion of purine bases.
    Metabolism, 2007
    Co-Authors: Terumi Kobayashi, Taku Inokuchi, Asako Yamamoto, Sumio Takahashi, Zenta Tsutsumi, Hiroki Saito, Yuji Moriwaki, Tetsuya Yamamoto
    Abstract:

    To determine whether an increase in the plasma concentration of uric acid by sucrose intake is ascribable to enhanced purine degradation and/or decreased Urinary Excretion of uric acid, we measured the plasma concentrations of purine bases (uric acid, hypoxanthine, and xanthine) and uridine, as well as the Urinary Excretion of purine bases in 7 healthy subjects before and after administering sucrose at 1.5 g/kg of body weight in 2 related experiments, with and without an administration of 300 mg of allopurinol. In addition, in the control experiment without an administration of sugar and with an administration of 300 mg of allopurinol, we measured the same parameters in those 7 subjects. Without added allopurinol, sucrose increased the plasma concentration of uric acid by 11% (P < .01) as well as that of uridine, although it did not significantly increase the plasma concentrations of hypoxanthine and xanthine or the Urinary Excretion of uric acid. On the other hand, the plasma concentration and Urinary Excretion of hypoxanthine were increased by 2.4-fold (P < .05) and 3.42-fold (P < .05), respectively, and the plasma concentration of xanthine was increased by 1.2-fold (P < .05) together with an increase in the plasma concentration of uridine in the experiment with allopurinol administration. In contrast, the plasma concentration and Urinary Excretion of uric acid and the Urinary Excretion of xanthine were not increased. In addition, in the control experiment, all parameters did not change significantly. These results indicate that purine degradation enhanced by sucrose plays a major role in the increased plasma concentration of uric acid.

  • Effect of octreotide acetate on the plasma concentration and Urinary Excretion of uridine and purine bases.
    Endocrine Journal, 2002
    Co-Authors: Tetsuya Yamamoto, Sumio Takahashi, Zenta Tsutsumi, Yuji Moriwaki, Toshikazu Hada
    Abstract:

    To determine the effect of octreotide acetate on Urinary Excretion of uric acid and plasma concentration of uridine, we subcutaneously administered octreotide acetate (1 microg/kg of body weight) to 5 healthy subjects. Ninety minutes after administration, octreotide acetate increased the plasma concentration of uridine by 15% and decreased the plasma concentration of glucagon by 24% and that of insulin to below the detection limits. In addition, octreotide acetate decreased the Urinary Excretion of uric acid, sodium, and chloride by 60%, 40%, and 38%, respectively, at 1 hour after administration. However, octreotide acetate did not affect the concentrations of hypoxanthine, xanthine, uric acid, cyclic AMP in plasma, lactic acid and pyruvic acid in blood, Urinary Excretion of hypoxanthine and xanthine, or creatinine clearance. From these results, we speculated that octreotide acetate decreases the Urinary Excretion of uric acid by decreasing the concentration of glucagon and/or Urinary Excretion of sodium, and increases the plasma concentration of uridine via decreased concentrations of glucagon and insulin.

  • Effect of norepinephrine on the Urinary Excretion of purine bases and oxypurinol
    Metabolism, 2001
    Co-Authors: Tetsuya Yamamoto, Sumio Takahashi, Zenta Tsutsumi, Yuji Moriwaki, Toshikazu Hada
    Abstract:

    To examine whether norepinephrine affects the plasma concentrations and Urinary Excretion of purine bases and oxypurinol, we orally administered allopurinol (300 mg) to 5 healthy subjects and 9 hours later intravenously administered norepinephrine (12 to 20 [mu ]g/kg body weight), which causes a more than 10 mm Hg increase in diastolic pressure for 2 hours. Norepinephrine decreased the Urinary Excretion of uric acid by 33% (P [lt ] .01), oxypurinol by 32% (P [lt ] .01), and xanthine by 51% (P [lt ] .01), as well as the fractional clearance of uric acid by 32% (P [lt ] .01), oxypurinol by 24% (P [lt ] .05), and xanthine by 21% (P [lt ] .05) when measured 1 to 2 hours after administration. These results indicate that norepinephrine decreases the Urinary Excretion of uric acid, oxypurinol, and xanthine, probably via hemodynamic change. It is also suggested that the hypouricemic effect of allopurinol may be more potent than that expected in gout patients with enhanced sympathetic tone, such as in salt-sensitive hypertension.

  • Effects of fructose and xylitol on the Urinary Excretion of adenosine, uridine, and purine bases.
    Metabolism, 1999
    Co-Authors: Tetsuya Yamamoto, Sumio Takahashi, Zenta Tsutsumi, Yuji Moriwaki, Jun-ichi Yamakita, Kazuya Higashino
    Abstract:

    To examine whether fructose and xylitol increase the plasma concentration and Urinary Excretion of adenosine, as well as uridine and purine bases (hypoxanthine, xanthine, and uric acid), we intravenously administered xylitol and, 2 weeks later, fructose, to five healthy subjects. Analyses of blood and urine samples obtained during these infusion studies demonstrated that fructose increased the Urinary Excretion of adenosine and uridine 11.9- and 105.5-fold, respectively, and caused only a small increase in the plasma concentrations of uridine and purine bases. It was further demonstrated that xylitol increased the Urinary Excretion of uridine 58.4-fold, with a marked increase in the plasma concentrations of purine bases and uridine but without an increase in the Urinary Excretion of adenosine. However, neither infusion increased the plasma concentration of adenosine. These results suggest that in addition to many organs, including the liver, fructose is significantly metabolized by an abrupt adenosine triphosphate (ATP) consumption in the kidney, leading to an increase in the Urinary Excretion of adenosine and uridine. They also suggest that xylitol is not significantly metabolized in the kidney.

Toshikazu Hada - One of the best experts on this subject based on the ideXlab platform.

  • Effect of octreotide acetate on the plasma concentration and Urinary Excretion of uridine and purine bases.
    Endocrine Journal, 2002
    Co-Authors: Tetsuya Yamamoto, Sumio Takahashi, Zenta Tsutsumi, Yuji Moriwaki, Toshikazu Hada
    Abstract:

    To determine the effect of octreotide acetate on Urinary Excretion of uric acid and plasma concentration of uridine, we subcutaneously administered octreotide acetate (1 microg/kg of body weight) to 5 healthy subjects. Ninety minutes after administration, octreotide acetate increased the plasma concentration of uridine by 15% and decreased the plasma concentration of glucagon by 24% and that of insulin to below the detection limits. In addition, octreotide acetate decreased the Urinary Excretion of uric acid, sodium, and chloride by 60%, 40%, and 38%, respectively, at 1 hour after administration. However, octreotide acetate did not affect the concentrations of hypoxanthine, xanthine, uric acid, cyclic AMP in plasma, lactic acid and pyruvic acid in blood, Urinary Excretion of hypoxanthine and xanthine, or creatinine clearance. From these results, we speculated that octreotide acetate decreases the Urinary Excretion of uric acid by decreasing the concentration of glucagon and/or Urinary Excretion of sodium, and increases the plasma concentration of uridine via decreased concentrations of glucagon and insulin.

  • Effect of norepinephrine on the Urinary Excretion of purine bases and oxypurinol
    Metabolism, 2001
    Co-Authors: Tetsuya Yamamoto, Sumio Takahashi, Zenta Tsutsumi, Yuji Moriwaki, Toshikazu Hada
    Abstract:

    To examine whether norepinephrine affects the plasma concentrations and Urinary Excretion of purine bases and oxypurinol, we orally administered allopurinol (300 mg) to 5 healthy subjects and 9 hours later intravenously administered norepinephrine (12 to 20 [mu ]g/kg body weight), which causes a more than 10 mm Hg increase in diastolic pressure for 2 hours. Norepinephrine decreased the Urinary Excretion of uric acid by 33% (P [lt ] .01), oxypurinol by 32% (P [lt ] .01), and xanthine by 51% (P [lt ] .01), as well as the fractional clearance of uric acid by 32% (P [lt ] .01), oxypurinol by 24% (P [lt ] .05), and xanthine by 21% (P [lt ] .05) when measured 1 to 2 hours after administration. These results indicate that norepinephrine decreases the Urinary Excretion of uric acid, oxypurinol, and xanthine, probably via hemodynamic change. It is also suggested that the hypouricemic effect of allopurinol may be more potent than that expected in gout patients with enhanced sympathetic tone, such as in salt-sensitive hypertension.