Urinary excretion of 6?-hydroxycortisol and the time course measurement of enzyme induction in man

1989 ◽  
Vol 36 (1) ◽  
pp. 39-46 ◽  
Author(s):  
E. E. Ohnhaus ◽  
A. M. Breckenridge ◽  
B. K. Park
Keyword(s):  
Urinary Excretion ◽  
Enzyme Induction ◽  
Time Course

Steroid induced changes of the renal kallikrein-kinin system in rats

1984 ◽  
Vol 107 (1) ◽  
pp. 131-140 ◽  
Author(s):  
G. Bönner ◽  
R. Autenrieth ◽  
M. Marin-Grez ◽  
G. Speck ◽  
F. Gross
Keyword(s):  
Urinary Excretion ◽  
Time Course ◽  
Urine Volume ◽  
Renin Angiotensin System ◽  
Sprague Dawley ◽  
Kinin System ◽  
Salt Loading ◽  
Renal Kallikrein ◽  
Kallikrein Kinin System ◽  
Kallikrein Activity

Abstract. In male Sprague-Dawley rats the influence of salt loading (1% NaCl), deoxycorticosterone acetate (2 × 15 mg/kg/day resp. 250 mg/kg sc), corticosterone (2 × 20 mg/kg/day sc) and adrenocorticosterone (0.5 mg/kg/day tetracosactid sc) on the activity of renal kallikrein and renal renin activity was investigated. Salt loading lowered renal kallikrein activity, deoxycorticosterone stimulated its activity and in combination they had no effect on renal kallikrein activity. The time course of kallikrein stimulation by deoxycorticosterone showed no relationship to the escape phenomenon of the kidney from the sodium retaining effect of the mineralocorticoid hormone. Reduction of endogenous mineralcorticoid hormones by adrenalectomy caused a marked reduction of urinary and renal kallikrein activity. Corticosterone suppressed the activity of the renal kallikrein-kinin system at the same time as the reduction in urinary aldosterone excretion. Adrenocorticotrophin caused the same decrease in the activity of renal kallikrein as corticosterone. Urinary aldosterone excretion, however, was significantly stimulated. Thus, the known positive correlation between kallikrein and aldosterone was missing. In all experiments the urinary excretion of kallikrein correlated highly with the kallikrein activity measured in renal cortical tissue. However, no correlation was found between kallikrein and urine volume or urinary excretion of sodium and potassium. In our experiments no relationship between the activity of the renin-angiotensin system and that of the renal kallikrein-kinin system was observed. Furthermore, no clear relationship was found between systemic blood pressure and the activity of the renal kallikrein-kinin system.

The Relationship between the Formation of Urea and Argininosuccinate in a Patient with Argininosuccinic Aciduria Studied with Labelled Precursors

1974 ◽  
Vol 46 (6) ◽  
pp. 715-727
Author(s):  
C. W. Crane ◽  
F. A. Jenner ◽  
R. J. Pollitt
Keyword(s):  
Oral Dose ◽  
Urinary Excretion ◽  
Time Course ◽  
Urea Cycle ◽  
Product Models ◽  
Ammonium Lactate ◽  
Argininosuccinic Aciduria ◽  
15N Urea ◽  
The Relationship

1. The time-course of urinary excretion of [15N]urea and [15N]argininosuccinate or [15N]arginine after an oral dose of [15N]ammonium lactate has been followed in patients with argininosuccinic aciduria and cystine-lysinuria respectively. The labelled argininosuccinate and arginine appeared more slowly than expected on simple precursor-product models. 2. In the patient with argininosuccinic aciduria, simultaneous ingestion of [15N]-ammonium lactate and [carbamoyl-14C]citrulline gave very different ratios of labelling with the two isotopes for urinary urea and argininosuccinate. Urinary argininosuccinate had not been in equilibrium with the urea precursor in this patient, but the plasma [14C]citrulline bore a reasonable precursor-product relationship to the urinary [14C]argininosuccinate. 3. Intravenous [guanidino-14C]arginine given to the patient with argininosuccinic aciduria resulted in a much higher degree of labelling of the plasma globulins than the albumin. This is consistent with a considerable turnover of hepatic arginine, as would be expected with a functioning Krebs-Henseleit urea cycle. 4. These results can be explained with a compartmentation model in which most of the urea is synthesized in the liver, but most of the urinary argininosuccinate is peripheral in origin.

URINARY EXCRETION OF INTRAVENOUSLY INJECTED 35S-SULPHATE AND 14C-UREA IN SHEEP

1975 ◽  
Vol 55 (2) ◽  
pp. 207-212 ◽  
Author(s):  
J. D. OLDHAM ◽  
G. W. MATHISON ◽  
L. P. MILLIGAN
Keyword(s):  
Urinary Excretion ◽  
Time Course ◽  
Microbial Growth ◽  
Diffusion Mechanism ◽  
Physiological Saline ◽  
Simple Diffusion ◽  
First Order ◽  
First Order Kinetics ◽  
The Difference

Sheep were injected intravenously with either 14C-urea (76.3–86.3 μc) orNa235SO4 (72.5–120.0 μc) in physiological saline. Total urinary excretion of label and, in one trial, the disappearance of label from plasma were measured for up to 106 h. Urinary recoveries were 64.9 ± 9.7% of injected 14C and 66.9 ± 12.7% of injected 35S. 35S was recovered more slowly than 14C; 99% of recovered label was collected in 36 ± 9 h after injection for 14C and in 84 ± 12 h for 35S. Disappearance of 14C from plasma approximated first-order kinetics but this was not true for 35S, which was apparently not excreted by a simple diffusion mechanism. The time course of 35S excretion from blood and into urine is discussed with reference to the potential of using the difference between intraruminally infused 35S and urinary 35S excretion as a measure of rumen microbial retention of 35S, and hence of microbial growth. It is concluded that large errors could be introduced into measurements of microbial growth by this method if that part of 35S that enters blood, but is not excreted into urine, is recycled within the animal to sites other than the rumen and retained therein.

Enzyme Induction and Serum and Lipoprotein Lipids: A Study of Glutethimide in Normal Subjects

1980 ◽  
Vol 58 (5) ◽  
pp. 419-421 ◽  
Author(s):  
C. H. Bolton ◽  
LYN Jackson ◽  
C. J. C. Roberts ◽  
M. Hartog
Keyword(s):  
Enzyme Induction ◽  
Time Course ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Lipoprotein Cholesterol ◽  
Total Serum ◽  
Total Serum Cholesterol ◽  
Low Density ◽  
Acid Excretion ◽  
Glucaric Acid

1. Serum and lipoprotein cholesterol and triglycerides were measured before, during and after the administration of glutethimide (500 mg daily) for 21 days to six healthy volunteer subjects. 2. Evidence of enzyme induction was provided by significant rises in d-glucaric acid excretion and antipyrine clearance. 3. Concentrations of total serum cholesterol, very-low-density-lipoprotein-, low-density-lipoprotein-and high-density-lipoprotein-cholesterol rose significantly during treatment. 4. The time course of these changes was delayed in comparison with the rise and fall in d-glucaric acid excretion. 5. There was no change in the triglyceride content of either whole serum or lipoprotein fractions at any time during the trial. 6. The study provides further evidence that enzyme-inducing agents cause a rise in certain lipid concentrations.

Urinary excretion of acetaminophen and its metabolites as studied by proton NMR spectroscopy.

1984 ◽  
Vol 30 (10) ◽  
pp. 1631-1636 ◽  
Author(s):  
J R Bales ◽  
P J Sadler ◽  
J K Nicholson ◽  
J A Timbrell
Keyword(s):  
Nmr Spectroscopy ◽  
Urinary Excretion ◽  
1H Nmr Spectroscopy ◽  
Time Course ◽  
Free Drug ◽  
Proton Nmr Spectroscopy ◽  
Drug Excretion ◽  
Clinically Normal ◽  
The Mean ◽  
Normal Men

Abstract Acetaminophen and its glucuronide, sulfate, N-acetyl-L-cysteinyl, and L-cysteinyl metabolites can be rapidly detected by 1H NMR spectroscopy of intact, untreated human urine. Study of the time course of excretion of these metabolites in five clinically normal men after ingestion of the usual 1-g therapeutic dose of the drug showed that the mean 24-h excretion of the drug and these metabolites as determined by NMR was 77.3% of the dose. Respective relative proportions of the above metabolites were 49.9%, 37.6%, 3.0%, and 9.5% (L-cysteinyl plus free drug). Excretion of some other metabolites in urine, including creatinine, citrate, hippurate, and sarcosine was measured concurrently. Excretion of creatinine and sarcosine was closely correlated.

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