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PubMed2002

[Appropriate administration schedule of D-penicillamine for pediatric Wilson's disease patients based on urinary copper excretion].

The purpose of this study was to increase the amount of copper excreted resulting from the administration of D-penicillamine(DP) in pediatric Wilson's disease(WD) patients. By measuring the urinary copper excretion after adjusting the administration schedules, the appropriate timing for DP administration was investigated. The subjects were three brothers with pediatric WD. The initial daily dose of DP was 5 mg/kg/day, and gradually increased to the maintenance dose of 20 mg/kg/day. Until the maintenance daily dose was reached, DP was administered 2 h after the morning and evening meal. After reaching the maintenance daily dose of DP, the appropriate timing for taking DP was investigated in both the morning and evening. Three schedules of DP administration were compared: 2 h after meals; 30 min before meals (with fasting); and 1 h before the morning and 1.5 before the evening meal (direction 1). The resulting urinary copper excretion on each dosing schedule was compared. Little difference was found in urinary copper excretion on the first two schedules, i.e., 2 h after meals and 30 min before meals. When DP was administered 30 min before meals, urinary copper excretion [microgram/day] was 1173 in the first brother, 918 in the second, and 875 in the third. When DP was administered according to direction 1, however, urinary copper excretion was increased significantly to 1701 in the first brother, 2701 in the second, and 3808 in the third. It is known that the efficiency of urinary copper excretion with DP administration depends on the maintenance of chelating ability after absorption from the gastrointestinal tract. Our results indicate that the excretion was lower when DP was administered 2 h after or 30 min before meals (with fasting), as recommended in the package insert. Thus to achieve better copper excretion efficiency, direction 1 is recommended for WD patients.

Biomarkers↗

PubMed2006

Analysis of pharmacokinetic data provided in Japanese package inserts and interview forms focusing on urinary excretion of pharmacologically active species.

In optimizing oral pharmacotherapy for patients with renal failure, information on actual urinary excretion ratio of the unchanged drug, which is obtained by dividing a urinary excretion ratio by a bioavailability after oral dose, is quite helpful. In addition, urinary excretion ratio of the active species is sometimes equally important where metabolites have a pharmacological potency. In the present study, we conducted a survey of Japanese package inserts and interview forms of drugs, which is being prescribed at the University of Tokyo Hospital, on pharmacokinetic data that enables an estimation of actual urinary excretion ratio. The total urinary excretion of a drug was documented in 70.1% of package inserts and 84.5% of interview forms, respectively. The total urinary excretion is often measured by radioactivity and thus includes its metabolites and degradation products. However, inclusion of degradation products/metabolites was described explicitly for 43.7% and 66.2%, and the absolute fraction of the unchanged drug or degradation product/metabolite was given only for 29.0% and 48.9% in package inserts and interview forms, respectively. The pharmacological activity of metabolite(s) was documented for 19.8% and 54.3%, and the oral bioavailability was described only for 5.7% and 30.6% in respective documents. For some drugs, the time period for the urine collection was too short to evaluate the urinary excretion ratio. With regard to 65 drugs (38.7%), more detailed information on urinary excretion was found in published books, but not provided in the package inserts or interview forms. It is hoped that more distinct and sufficient descriptions on the urinary excretion and bioavailability will be associated to the package inserts and the interview forms in future, for safe and efficient use of prescription drugs.

Administration, Oral↗

PubMed1981

A circadian variation in the excretion of urinary kinin, kallikrein and prostaglandin E in normal volunteers.

The present study shows that there is a circadian variation in the excretion of urinary kinin, kallikrein and prostaglandin E (PGE) as well as urine flow, urinary sodium excretion and urinary potassium excretion in recumbent healthy volunteers. The present data, that the acrophase of urinary kallikrein excretion was 1.5 hr later than that of plasma aldosterone concentration (PAC) and that a significant positive correlation was found in circadian variations between urinary kallikrein and PAC, suggest that the circadian variation of urinary kallikrein excretion may be regulated by aldosterone. The pattern of circadian variation of average urinary kinin excretion coincided with those of average urine flow, urinary sodium excretion and urinary PGE excretion, suggesting that renal kinin and PGE may be involved in the regulation of water-sodium excretion. The present data that the phase of circadian variation of urinary kinin was delayed from that of urinary kallikrein and that there was a mirror image between the circadian variation in urinary kinin and kallikrein suggest that there may be a feedback mechanism in renal kallikrein-kinin system.

Adult↗

PubMed1992

Relationship of urinary serotonin excretion to cigarette smoking and respiratory symptoms. The Normative Aging Study.

The relationship of 2-h urinary excretion of serotonin and 5-hydroxyindoleacetic acid (5-HIAA) to cigarette smoking and respiratory symptoms was examined among 631 male participants in the Normative Aging Study (age range, 44 to 85 years). The amount of serotonin excreted in urine was inversely related to age (p less than 0.001). Mean 2-h excretion of serotonin varied from 8.01 micrograms for men 40 to 49 years of age to 5.84 micrograms for those 70 years of age or over. No clear relationship was evident between the amount of 5-HIAA excreted in urine and age. After adjustment for age, current smokers were found to excrete more serotonin (p less than 0.001) and 5-HIAA (p = 0.001) than never smokers. Former smokers did not differ significantly from never smokers in these respects. After adjustment for age and smoking status in a multivariate model, chronic cough was a significant predictor of serotonin excretion (p = 0.005); chronic cough was less predictive of 5-HIAA excretion (p = 0.07). Other respiratory symptoms were unrelated to urinary excretion of serotonin and 5-HIAA. The mechanisms underlying the observed relationships of urinary serotonin and 5-HIAA excretion to smoking and to chronic cough and their potential relevance to chronic bronchitis remain to be determined.

Age Factors↗

PubMed1983

[Urinary excretion of hydroxyproline in parathyroid disorders, with special reference to its changes before and after parathyroidectomy in primary hyperparathyroidism].

It is possible to assess bone resorption from a determination of urinary excretion of hydroxyproline, which is the specific amino-acid of collagen. As dietary collagen affects 24-hour urinary excretion of hydroxyproline, it has been stated that the urine should be collected under a gelatin-free diet. A new sampling method was described in the present paper for the determination of hydroxyproline in urine, which could eliminate the affection of dietary collagen by simple fasting. The method was useful for the evaluation of bone metabolism in patients with parathyroid disorders. 10 patients with primary hyperparathyroidism (3 skeletal types and 7 non-skeletal types), 3 patients with idiopathic hypoparathyroidism and 5 normal subjects were studied. It was found that the urinary excretion of hydroxyproline increased at night and diminished during the day in patients with primary hyperparathyroidism as well as in normal subjects, but this diurnal rhythm was not clear in a patient with idiopathic hypoparathyroidism. A pilot study revealed that 10 g gelatin administered orally did not affect the urinary excretion of hydroxyproline after a 12-hour fast. Therefore, 2-hour urine samples (700 h-900 h) were collected, and blood samples were drawn at 800 h after a 13-hour fasting from 1800 h on the previous day to 700 h in the morning studied. The urinary excretion of hydroxyproline was expressed as follows: HOP (microgram/ml)/Cr(mg/dl). The 2-hour urinary excretion of hydroxyproline thus determined was highly correlated with that determined in 24-hour urine collected under a gelatin-free diet (r = 0.995, p less than 0.001) and with the total serum alkaline phosphatase activity (r = 0.987, p less than 0.001). The levels of 2-hour urinary excretion of hydroxyproline in normal subjects were 0.18-0.28 in range, and those in patients with the skeletal type of primary hyperparathyroidism were high. However, the levels were not always higher than those in the patients with the non-skeletal type, in which cases the 2-hour excretion of hydroxyproline was higher than 0.50 except in one patient. The 9 patients with primary hyperparathyroidism who had elevated levels of the 2-hour urinary excretion of hydroxyproline showed tetany after parathyroidectomy.(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗

PubMed1986

Circadian rhythms of 6-sulphatoxy melatonin, cortisol and electrolyte excretion at the summer and winter solstices in normal men and women.

Urinary excretion of 6-sulphatoxy melatonin, cortisol, potassium and sodium was monitored at four hourly intervals for 24 h in 30 normal subjects at the summer and winter solstices. The 24 h profiles were fitted to sine curves and mean 24-h excretion, time of maximum excretion and amplitude of the curves compared. The excretion of 6-sulphatoxy melatonin was remarkably stable at the two times of the year (24-h excretion 108 +/- 6.3 nmol in summer and 105 +/- 6.3 nmol in winter, mean +/- SEM). The time of maximum excretion was significantly delayed in winter by 1 h and 40 min. Urinary cortisol excretion was significantly higher in winter, however, the amplitude was unaltered. The time of maximum excretion of cortisol was significantly delayed by 1 h and 34 min. Postassium and sodium excretion were both unaffected by seasonal influences. These results contrast with results in some animal species in which the duration of the melatonin signal is thought to be the key determinant in subsequent melatonin action. In humans it is likely that the phasing of the melatonin rhythm is of prime importance.

Adult↗

PubMed2001

Variations in urinary iodine excretion and thyroid function. A 1-year study in healthy men.

OBJECTIVE: The iodine intake level in a population is determined in cross-sectional studies. A fraction of samples with iodine content below a certain level, e.g. 25 microg/l, may suggest iodine deficiency in part of the population. However, urinary iodine varies considerably from day to day and the fraction of low samples caused by dispersion remains unsettled. DESIGN: A longitudinal study of 16 healthy men living in an area of mild to moderate iodine deficiency. METHODS: We measured urinary iodine and creatinine concentrations, and serum TSH, total thyroxine (T4), free T4 index and total tri-iodothyronine (T3) in samples collected monthly for 1 year. RESULTS: Average urinary iodine excretion was 57.0 microg/l (49.1 microg/24 h (corrected for creatinine excretion)) and varied from 29 to 81 microg/l (28 to 81 microg/24 h) between participants. Individual samples varied between 10 and 260 microg/l, and the variation around the mean was 2.4 times larger when calculated for the 180 individual samples compared with the 15 average annual values (1.7 times larger for estimated 24 h iodine excretion values). The fraction of individual samples below 25 microg/l was 6.7% (7.2% < 25 microg/24 h), whereas none of the participants had average iodine excretion below 25 microg/l or 25 microg/24 h. Participants with average annual iodine excretion below 50 microg/24 h had a negative correlation between iodine excretion and TSH, whereas a positive correlation was observed when average annual iodine excretion was above this level. CONCLUSIONS: Seven per cent of individual urine samples indicated severe iodine deficiency without this being present in the group studied. Dispersion was reduced by 24% when using estimated 24 h urinary iodine excretion rather than urinary iodine concentration. Participants with moderate iodine deficiency (average annual urinary iodine excretion 25-50 microg/24 h) showed clear signs of substrate deficiency for thyroid hormone synthesis while participants with mild iodine deficiency (50-100 microg/24 h) did not.

Adult↗

PubMed1977

Effects of 1-Sar-8-Ile-angiotensin II on urinary prostaglandin excretion in patients with essential hypertension.

To investigate the interaction between the renin angiotensin aldosterone system and the renal prostaglandin (PG), urinary excretion of PGE, urinary excretion of main urinary metabolite (MUM) of PGF2a, urinary excretion of aldosterone, and plasma renin activity were measured before and after infusion of 1-Sar-8-Ile-Angiotensin II, a specific competitive inhibitor of angiotensin II, in 18 patients with essential hypertension under normal and low sodium diets. The values of urinary sodium excretion in these patients before the infusion of the peptide were 160.8 +/- 13.3 and 27.0 +/- 2.7 mEq per day on normal and low sodium diet, respectively. On normal sodium diet, urinary excretion of PGE was found to correlate with the level of plasma renin activity before the infusion (r = 0.6977, p less than 0.01), and it was decreased slightly from 0.37 +/- 0.05 ng/min to 0.26 +/- 0.04 ng/min after the infusion of the antagonist. On low sodium diet, urinary excretion of PGE was not significantly changed by the infusion of the peptide and showed no correlation with the level of plasma renin activity before the infusion, while urinary excretion of PGE showed a significant correlation with the excretion of urinary aldosterone (r = 0.6719, p less than 0.02). Excretion of PGF2aMUM decreased after the infusion of this peptide on both sodium diets, but the changes were not statistically significant. The present data suggest that angiotensin II influences the synthesis or release of renal PG in patients with essential hypertension on normal sodium diet, but not when they are on low sodium diet.

Adolescent↗

PubMed1993

Tissue concentration and urinary excretion pattern of sulfofluorescein by the rat kidney.

In order to find a fluorescein analog that is excreted in a way similar to p-aminohippurate (PAH) and is suitable to register excretion into the urine and also to monitor continuously the concentration within cortical tissue, the interference of fluorescein, sulfofluorescein (SF), and fluorescein-5(6)-sulfonate with the contraluminal transport systems of PAH, succinate, and sulfate and with the luminal transport system of sulfate and lactate was evaluated. All three substances exerted a strong inhibitory potency against contraluminal PAH uptake (apparent Ki, 0.06 to 0.1 mmol/L) and also showed a moderate to small inhibitory potency against contraluminal sulfate transport (apparent Ki, 0.7 to 5.3 mmol/L). None of the three substrates interacted with the contraluminal dicarboxylate transport. Luminally, fluorescein and SF interacted with the lactate transporter (apparent Ki, approximately 3.0 mmol/L), whereas SF and fluorescein-5(6)-sulfonate had a very weak inhibitory potency against luminal sulfate transport (apparent Ki, 30 to 40 mmol/L). Because of its relatively low interference with the contraluminal sulfate transport, we preferred SF in the following study (protein binding, 88%) over fluorescein-5(6)-sulfonate (protein binding, 43.3%) and fluorescein (protein binding, 77.3%). A bolus injection of SF was given together with [14C]inulin into the jugular vein to rats in mannitol diuresis. Excretion of both substances in the urine was measured in 5-min samples. Fluorescence of the kidney surface was monitored at the exposed kidney with a photocell (excitation light, 470 nm; emission light, 530 nm). The effect of interfering substances was evaluated by their application 1 min before, simultaneously, or 1 min after SF bolus injection. PAH < probenecid < apalcillin inhibited SF excretion in the urine and, to a similar degree, SF fluorescence in cortical tissue. Inhibition was strongest when the substances were given simultaneously with SF. With the injection of alpha-ketoglutarate, glutarate, and succinate, an increase of SF excretion in the urine and, partially also, of SF content in tissue was seen. Tetrafluorosuccinate and mercaptosuccinate inhibited urinary SF excretion and tissue fluorescence strongly. Therefore, SF secretion is completely inhibited whereas filtration remained unaffected. The injection of acetate, lactate, and pyruvate as well as of 2-chloropropionate and thiosulfate did not change urinary excretion and tissue fluorescence of SF significantly. In SF-preloaded animals, the injection of probenecid, apalcillin, tetrafluorosuccinate, and mercaptosuccinate caused an immediate decrease of cellular SF content, whereas the injection of glutarate caused an increase. SF fluorescence in tissue was linearly related to urinary excretion of SF, whereas urinary excretion of inulin was barely affected.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

PubMed1989

Sulfate and taurine excretion in rats after L-cysteine administration.

Excretion of sulfate and taurine, two major metabolites of sulfur, was examined in rats to study the nutritional status of sulfur metabolism in the mammals. Rats maintained on a conventional laboratory diet excreted 1.83 +/- 0.14 mmol of free sulfate and 229.0 +/- 75.3 mumol of taurine/kg of body weight per day. When the diet was changed to a synthetic 25% casein diet, the taurine excretion decreased to 15% of the previous daily excretion, but sulfate excretion decreased only slightly. These decreased levels returned to the original levels when 5 mmol of L-cysteine/kg of body weight was administered into the stomach through a catheter. One week after the first L-cysteine administration, when sulfate and taurine excretion had returned to the original levels, 5 mmol of L-cysteine/kg of body weight was administered likewise. The rats excreted sulfur corresponding to about 95% of L-cysteine administered in the form of free sulfate and taurine within a few days following L-cysteine administration, and sulfate excretion was 3.5 times more than taurine excretion. These results seem to suggest that, in rats, sulfur metabolism is in a state of equilibrium and that sulfate is formed preferentially to taurine.

Animals↗

PubMed2005

Molecular factors and mechanisms affecting iron and other metal excretion or absorption in health and disease: the role of natural and synthetic chelators.

The maintenance of iron and other essential metal ion balance in humans is based on the presence of homeostatic mechanisms of regulatory absorption, storage, re-utilisation and excretion. There are a number of factors and mechanisms that can affect the level of iron excretion or absorption and overall body iron stores. Net iron loss due to increased iron excretion by comparison to dietary iron absorption is considered as one of the causes of iron deficiency anaemia. Body iron loss greater than normal has been shown in many other conditions. These include the increase in urinary iron excretion observed in iron loaded patients, the substantial reduction in serum ferritin and liver iron of ex-thalassaemia patients several years following bone marrow transplantation and the increase in iron excretion in normal individuals following long term sport activities. There are differences in the metabolism, mode of action, interactions with the iron pools and routes of iron excretion, of the iron chelating drugs deferiprone (L1), deferoxamine and other experimental chelators such as ICL670 in iron-loaded patients. Naturally occurring chelators and some synthetic drugs are known to bind iron and affect iron absorption and excretion. The molecular characteristics of naturally occurring or synthetic chelators can influence other aspects of iron metabolism in addition to iron absorption or excretion. Similar mechanisms and factors can affect the metabolism of other essential metals. The understanding of the mechanisms involved in iron excretion and their overall effects on body iron levels can facilitate the design of new chelators and improved therapeutic protocols for the treatment of conditions of iron and other metal metabolic imbalance and toxicity.

Benzoates↗

PubMed1989

Urinary excretion of angiotensin-converting enzyme in NIDDM patients with nephropathy.

Twenty-four-hour urinary excretion of angiotensin-converting enzyme (ACE) was investigated in relation to that of albumin and beta 2-microglobulin (beta 2M) in 25 non-insulin-dependent diabetes mellitus (NIDDM) patients without nephropathy, 13 NIDDM patients with incipient nephropathy, 18 NIDDM patients with overt nephropathy, and 14 nondiabetic subjects. NIDDM patients without nephropathy and nondiabetic subjects were similar in albumin, beta 2M, and ACE excretion. NIDDM patients with incipient nephropathy had elevated albumin excretion (P less than .01) and similar beta 2M and ACE excretion compared with nondiabetic subjects. On the other hand, NIDDM patients with overt nephropathy had elevated albumin, beta 2M, and ACE excretion compared with nondiabetic subjects (P less than .01). In all NIDDM patients studied, a positive correlation was found between ACE excretion and albumin excretion (r = 0.76, P less than .001) or beta 2M excretion (r = 0.52, P less than .01). These data suggest that elevated ACE excretion in NIDDM patients with overt nephropathy may be reflective of renal tubular damage.

Albuminuria↗

PubMed2004

Parallel increase in urinary excretion rates of immunoglobulin G, ceruloplasmin, transferrin, and orosomucoid in normoalbuminuric type 2 diabetic patients.

OBJECTIVE: Increased urinary excretions of several plasma proteins with different molecular radii <55 A and different isoelectric points (pI), such as IgG, ceruloplasmin, transferrin, and orosomucoid, have been independently reported to precede the development of microalbuminuria in diabetic patients. We examined whether increases in urinary excretions of these proteins would be in parallel in the same patient. RESEARCH DESIGN AND METHODS: Urinary excretion rates of proteins mentioned above in timed overnight urine samples were evaluated in 61 normoalbuminuric type 2 diabetic patients (group D) aged 40-60 years and in 17 age-matched control subjects (group C). RESULTS: The excretion rates of these proteins were significantly higher in group D than in group C. These exhibited a strong linear correlation with each other and had a weak correlation with the excretion rate of N-acethylglucosaminidase. The excretion rate of alpha2-macroglobulin with large molecular radii of 88 A was not different between groups C and D, nor did they have any correlations with the excretion rates of the other proteins. Creatinine clearance and blood pressure levels in group D were significantly higher than those in group C. CONCLUSIONS: In normoalbuminuric diabetic patients, excretion rates of plasma proteins with molecular radii <55 A increased in parallel with each other. In view of our previous finding that urinary excretions of these plasma proteins selectively increased in parallel with enhanced glomerular filtration rate after acute protein loading, the present finding may be explained by renal hemodynamic changes, such as increased intraglomerular hydraulic pressure.

Adult↗

PubMed2002

Effects of dietary protein and fermentable fiber on nitrogen excretion patterns and plasma urea in grower pigs.

Effects of dietary protein concentration (high, 18.5; low, 15.7%) and fermentable fiber (control; soyhulls, SH; and sugar beet pulp, SBP) on N excretion patterns and plasma urea were tested in a 2 x 3 factorial arrangement. The objectives were: 1) to determine if reduced dietary protein together with fermentable fiber would reduce urinary N excretion further than a single diet manipulation, 2) to determine if effects of diet manipulations were similar between pigs with restricted and free access of feed, and 3) to further develop predictions of urinary N excretion using plasma urea. Diets were formulated to 3.30 Mcal digestible energy (DE)/kg and 2.4 g of digestible lysine per Mcal DE, and supplemented with lysine, methionine, tryptophan, threonine, isoleucine, leucine, or valine to ensure meeting an ideal AA profile. Pigs (30.5 +/- 3 kg; n = 36) were housed in metabolism crates with restricted access to feed (3 x 110 kcal DE/kg BW(0.75)) from d 1 to 18, and free access from d 19 to 26. Feces and urine were collected from d 15 to 18 and d 23 to 26, and blood was sampled on d 17 and 25. With restricted access to feed, urinary N was reduced 28% and N retention was reduced 12% for the low- compared to high-protein diet (P < 0.01; as g/d). Fecal N was increased 4% units for SH and 6.5% units for SBP (P < 0.01; as % of N intake) and urinary N was reduced 5% units for SH (P < 0.10) and 9% units for SBP (P < 0.05) compared to the control. With free access to feed, urinary N was reduced 27% (P < 0.05; as g/d) and N retention was reduced 7% (P < 0.10) for the low- compared to high-protein diet. Fecal N was increased 5% units for SH and 9% units for SBP (P < 0.001; as % of N intake), and urinary N was reduced 9% units for SH and 10% units for SBP (P < 0.01) compared to the control. For either restricted or free access to feed, fermentable fiber did not affect N retention (P > 0.10). A protein x fiber interaction was not observed for urinary N excretion (P > 0.10), indicating that reducing dietary protein and including fermentable fiber reduced urinary N excretion in an additive manner. Daily urinary N excretion was related positively and linearly with plasma urea in pigs with free access to feed (R2 = 0.71; at 0800). In summary, reduction of dietary protein reduced urine N excretion, and fermentable fiber shifted N excretion from urine to feces. Effects of dietary protein and fermentable fiber on reducing urinary N excretion are additive.

Animals↗

PubMed2000

Urinary excretion of aquaporin-2 in pathological states of water metabolism.

Aquaporin-2 (AQP-2) is an arginine vasopressin (AVP)-regulated water channel in renal collecting duct cells. Approximately 3 % of AQP-2 in collecting duct cells is excreted into urine. Urinary excretion of AQP-2 varies widely in different physiological conditions, and it has a positive correlation with plasma AVP levels. Urinary excretion of AQP-2 was significantly increased by the single injection of AVP in patients with central diabetes insipidus. The urinary excretion of AQP-2 was one-eighth over in patients with central diabetes insipidus and three times greater in patients with impaired water excretion than that in normal subjects. In a hypertonic saline test, the urinary excretion of AQP-2 promptly increased 6-12-fold in normal subjects, but remained low in patients with central diabetes insipidus. In addition, exaggerated urinary excretion of AQP-2 persisted after an acute water load in patients with impaired water excretion. These results indicate that urinary excretion of AQP-2 is a potent marker for the diagnosis of water metabolism disorders dependent on AVP.

Animals↗

PubMed1987

Dietary sodium intake and urinary dopamine and sodium excretion during the course of blood pressure development in Dahl salt-sensitive and salt-resistant rats.

Recent studies have suggested that dopamine (DA) formed within the kidney may play an important role in promoting sodium excretion, and that renal production and excretion of DA is determined by dietary sodium intake. Inasmuch as increased sodium consumption produces hypertension in Dahl salt-sensitive (DS) rats but not in Dahl salt-resistant (DR) rats, the present study was designed to examine the relationship between sodium consumption and urinary excretion of DA in these rats. DS and DR rats were placed on either high sodium chloride (8%) or low sodium chloride (0.4%) diets at 4 weeks of age and their systolic blood pressure (SBP), urine volume, urinary sodium and catecholamine excretion were measured once every week for the next 4 weeks. High sodium chloride diet increased SBP in DS rats at 6 weeks of age and SBP continued to rise until they were 8 weeks old. The SBP of DR rats did not reach hypertensive levels when they were given high sodium chloride diet. The SBP of DS rats on low sodium chloride diet was significantly higher than DR rats on the same diet. The urinary DA excretion increased with age in all four groups of rats and was similar when they were 8 weeks old. However, both DS and DR rats on high sodium chloride diet excreted greater amounts of sodium and had increased urine volume compared to the DS and DR rats on low sodium chloride diet. There were no significant differences in urinary NE or E excretion in these four groups of rats. Kidney levels of DA and NE were significantly lower in DS compared to DR rats on high sodium chloride diet. These results show that although there are no differences in urinary DA excretion between rats on low and high sodium intake, both DS and DR rats on high sodium chloride diet are able to exhibit a natriuretic response. The DS rats eliminate sodium at the expense of an elevated SBP whereas DR rats stay normotensive. Therefore, it appears that alterations in mechanisms controlling renal vascular resistance rather than sodium excretion are responsible for the development of hypertension in DS rats.

Animals↗

PubMed1979

The phosphorus excretion pattern and balance during one egg cycle of the laying hen fed a phosphorus deficient diet with or without a single dose of phosphoric acid.

A balance trial was conducted to study the phosphorus excretion pattern of laying hens in relation to egg cycle. Excreta were collected quantitatively at 4, 8, 12, and 24 hr after oviposition. The amount of feed consumed corresponding to the excreta collected at a specific time interval was calculated using chromic oxide as a marker. The percent recovery of chromic oxide with laying hens was 73.97 +/- .56%. The maximum apparent digestibility of the dietary phosphorus, all of plant origin, was estimated to be 28.9 +/- 3.1% during 0 to 4 hr after oviposition when the endogenous excretion of phosphorus was theoretically minimized. Laying hens fed a diet containing .30% phosphorus excreted 24.3 mg less phosphorus than intake during the day, indicating that hens had to withdraw approximately 100 mg of phosphorus from their body to produce an egg. These hens excreted 63.1 +/- 27.0 mg of endogenous phosphorus during the 24 hr period, most of which was excreted during the period between 12 to 24 hr after oviposition of the previous egg. The excretion pattern of phosphorus was closely related to the egg laying cycle of the hen. Hens dosed with 100 mg of phosphorus, as a phosphoric acid solution, excreted more phosphorus than the undosed control birds. Approximately 45 mg of 100 mg of the phosphorus dose were excreted during the 24 hr period. At least 84.8 mg of the dosed phosphorus were absorbed within 12 hr and a part of it was excreted during the later period. Data indicated that the true absorption rate of the dosed phosphorus might have been much faster.

Animal Feed↗

PubMed2005

Tissue distribution and excretion of 125I-lidamycin in mice and rats.

AIM: To investigate the tissue distribution, urinary and fecal excretions of (125)I-lidamycin ((125)I-C-1027) in mice and its biliary excretion in rats. METHODS: The total radioactivity assay (RA method) and the radioactivity assay after precipitation with 200 mL/L trichloroacetic acid (TCA-RA method) were used to determine the tissue distribution, and the urinary and fecal excretions of (125)I-C-1027 in mice and its biliary excretion in rats. RESULTS: Tissue concentrations reached the peak at the fifth minute after administration of (125)I-C-1027 to mice. The highest concentration was in kidney, and the lowest in brain at all test-time points. The organs of the concentrations of (125)I-C-1027 from high to low were kidney, lung, liver, stomach, spleen, uterus, ovary, intestine, muscle, heart, testis, fat, and brain in mice. The accumulative excretion amounts of 0-24 h, and 0-96 h after administration of (125)I-C-1027 were 68.36 and 71.64% in urine, and 2.60 and 3.21% in feces of mice, respectively, and the accumulative excretion amount of 0-24 h was 3.57% in bile in rats. CONCLUSION: Our results reflect the characteristics of the tissue distribution, urinary and fecal excretions of (125)I-C-1027 in mice and the biliary excretion of (125)I-C-1027 and its metabolites in rats, and indicate that (125)I-C-1027 and its metabolites are mainly distributed in kidney, and excreted in urine.

Aminoglycosides↗