Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “EXCRETION”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,081 records · Page 60Linked to original sources
PubMed1982

The effect of sex, height and time of day on the excretion of glycosaminoglycans and the consequences.

A diurnal rhythm in the excretion of glycosaminoglycan-derived uronic acid with an increased excretion during daytime has been found in adults. Due to this rhythm a 24-h excretion was established as the optimum measurement of glycosaminoglycan turnover in tissue. Neither the excretion of uronic acid nor the uronic acid/creatinine ratio in the morning urine could predict the 24-h excretion of glycosaminoglycans as estimated by a statistical model. This model may also be of general interest in similar clinical problems. Compared with males, females had a lower excretion of glycosaminoglycans. Part of this discrepancy reflected a sex-difference in height, which was shown to be positively correlated with the excretion. On the other hand, the uronic acid/creatinine ratio was not influenced by height or sex. Body mass, age and urine output did not influence the ratio or the excretion of uronic acid.

Adolescent↗
PubMed1980

Circadian variations in urine excretion in chronic renal failure.

The pattern of urine excretion over 24 hours has been studied in nineteen patients with stable chronic renal failure of varying severity and due to a variety of renal disorders. The patterns were compared with those in eighteen health control subjects of similar age. The 24 hour urine volume was not significantly greater in the patients (1608 +/- 112 compared with 1710 ml +/- 169). A lower urine concentration (341 +/- 79 mOsm compared with 430 +/- 160 mOsm/kg) was associated with a lower total 24 hour solute excretion (596 +/- 224 compared with 699 +/- 169 mOsm/24 hours). Frequency of micturition, expressed in relation to periods of 24 hours, was similar (6.8 +/- 0.6 compared with (6.4 +/- 0.5). There was an alteration in the normal pattern of urine flow, with more urine at night and less in the day. Nocturia, a consistent feature of the patients with renal failure is due to reversal of the normal pattern and not to an increased volume of urine or increased frequency of micturition. The time of onset of decreased urine excretion during the day was associated with the change from recumbency to activity. The morning antidiuresis, and the nocturnal diuresis, are associated with, and probably the result of, changes in sodium and total solute excretion. The circadian rhythm of potassium excretion remained normal in chronic renal failure, except in very severe renal failure when it was reversed. Alterations in sodium, total solute and water excretion were associated with changes in creatinine excretion and were observed even in mild renal failure. In some patients, studied just before commencing regular dialysis, renal function would have been adequate for reasonable health had the rates of excretion observed at night persisted throughout the 24 hours. Nocturia, in nineteen patients with chronic renal failure, was due to a change in the circadian pattern of urine flow; it is suggested that this results, at least in part, from an inability to respond normally to changes from recumbency to activity.

Adult↗
PubMed1994

[Studies on urinary protein components in renal diseases in children. I--Characteristics of urinary protein components in renal diseases in children, with a focus on the relationship between IgA nephropathy and urinary IgA excretion].

Urinary protein components in children with renal disease were analyzed by the Reversed-Single Radial Immunodiffusion (R-SRID) method. The results were as follows: (1) In idiopathic nephrotic syndrome, the percentage of urinary albumin excretion was very high (79.5%). Urinary IgA excretion was 0.1% and IgG excretion was 1.6%, hence the excretion of these high-molecular-weight proteins amounted to 1.7% of the total urinary protein. (2) In membranous glomerulonephritis, urinary IgA was not detected, whereas the percentage of urinary IgG excretion was high (5.4%). (3) The percentage of urinary IgA excretion was higher in IgA nephropathy (IgAN) and Henoch-Schönlein purpura nephritis (HSPN) (2.4%, 1.6% respectively) than in other diverse renal diseases. (4) The percentage of urinary IgA excretion was correlated significantly with the serum IgA concentration in IgAN and HSPN (P < 0.001), but there was no such correlation in other diverse renal diseases. (5) In IgAN, the percentage of urinary IgA excretion was significantly higher in the subgroup with a duration of less than one year from the onset (3.6%) than in the subgroup with a duration longer than one year (1.5%) (p < 0.01).

Adolescent↗
PubMed1994

Body lead stores and urate excretion in men with chronic renal disease.

OBJECTIVE: To determine the relationship of urate excretion to body lead stores in patients with chronic renal disease without previous lead exposure. METHODS: We compared 40 male subjects in 3 groups, on the basis of their serum creatinine and histories of gout, with serum urate, creatinine clearance, urate clearance, daily urate excretion, fractional urate excretion, and body lead stores. Group 1 consisted of 10 patients with normal serum creatinine levels and no evidence of gout. Group 2 contained 10 men with gout and abnormal serum creatinine levels. Group 3 included 20 subjects with abnormal serum creatinine levels and no evidence of gout. All patients received EDTA mobilization tests and 72 h urine collections. The total amount of lead excreted over 72 h was estimated as the body lead stores. An ANOVA test with Fisher pairwise least significant difference, correlation coefficients, and multiple linear regression test were used to measure any statistical significance among these variables. A p value < 0.05 was considered significant. RESULTS: Lead stores and serum urate were significantly higher in gouty patients with renal insufficiency than those of other groups, but the urate excretion of gouty patients was not relatively increased. Not only was there a significant correlation between creatinine clearance and urate excretion, but body lead stores also appeared to be negatively related to urate excretion in our patients, even though body lead stores in these subjects were within the normal range. CONCLUSION: Our findings suggest that lead may play a role in gouty patients with impaired renal function and chronic low level environmental lead exposure may subtly affect urate excretion in patients with chronic renal disease.

Adult↗
PubMed1994

Vagal dysfunction and impaired urinary sodium and water excretion in cirrhosis.

OBJECTIVE: To evaluate the possible role of vagal impairment in the disturbances of urinary sodium and water excretion observed in cirrhosis. METHODS: Standard cardiovascular reflex tests were used to assess Autonomic function in 11 cirrhotic patients, and the response to an acute intravenous water load was determined. Changes in plasma noradrenaline, antidiuretic hormone, renin, and atrial natriuretic peptide also were evaluated. RESULTS: Patients with vagal dysfunction were shown to have significantly impaired urinary sodium and water excretion, compared with those whose cardiovascular tests were normal (5-h urinary sodium excretion, 32.3 +/- 9.0 vs. 69.4 +/- 12.7 mmol, p < 0.05; % water load excreted at 5 h, 67.8 +/- 10.5 vs. 109.2 +/- 3.67%, p < 0.008). This was associated with higher circulating noradrenaline, renin, and antidiuretic hormone levels after the water load in the vagal dysfunction group. Urinary sodium excretion correlated with the heart rate variation on deep breathing (r = 0.74, p < 0.013) and the heart rate response to atropine (r = 0.75, p < 0.020); the % water load excreted correlated with the number of abnormal cardiovascular tests in each patient (rS = 0.67, p < 0.02). Although patients with vagal abnormalities had worse liver function, urinary sodium and water excretion correlated better with parasympathetic tests than with standard parameters of hepatic function. CONCLUSIONS: The presence of vagal impairment in cirrhosis appears to be associated with impaired urinary sodium and water excretion, as well as disturbances in circulating vasoactive hormones. These findings could be due to an afferent defect resulting in diminished inhibitory input from intrathoracic volume and arterial baroreceptors, although a confounding effect of worse hepatic function in patients with vagal impairment cannot be excluded.

Atrial Natriuretic Factor↗
PubMed1993

Bile acid excretion and cholesterol 7 alpha-hydroxylase expression in hypercholesterolemia-resistant rabbits.

We have developed a partially inbred substrain of New Zealand white rabbits (CRT/mlo) that are resistant to the hypercholesterolemia that accompanies cholesterol feeding to normal rabbits. The plasma cholesterol concentration of normal rabbits increases dramatically from about 30 mg/dl to > 300 mg/dl after they are fed a 0.1% cholesterol-enriched diet for 3-4 months. Cholesterol-fed CRT/mlo animals, however, maintain a cholesterol level of about 30 mg/dl during the entire cholesterol feeding period. In addition to the low plasma cholesterol level, measurements of cellular cholesterol indicate that the hepatic cholesterol content of the cholesterol-fed resistant rabbit remains markedly lower than it does in normal animals fed the same diet. The only mechanism for removal of significant quantities of cholesterol carbon from the body is via the fecal excretion of cholesterol, neutral sterol metabolites, and bile acids. In comparison to the basal, low-cholesterol diet, we observed that cholesterol-fed resistant rabbits had increased excretion of lithocholic acid, while excretion of this bile acid by cholesterol-fed normal rabbit remained similar to basal diet levels. Deoxycholic acid excretion, the other main bile acid excreted in the feces of rabbits, was decreased in response to cholesterol challenge in animals with either resistant or normal phenotypes, but the decrease was significantly less in the resistant rabbits. Thus, the resistant rabbits excreted relatively more lithocholic and deoxycholic acid than did the cholesterol-fed normal rabbit. The difference in bile acid excretion was also manifest by a higher than normal level of cholesterol 7 alpha-hydroxylase activity and cholesterol 7 alpha-hydroxylase mRNA in the livers from resistant versus normal rabbits. As cholesterol 7 alpha-hydroxylase is the putative rate-limiting step of bile acid synthesis, we believe that the increased excretion of bile acids by resistant animals is due, at least in part, to increased levels of cholesterol 7 alpha-hydroxylase expression.

Animals↗
PubMed1993

Evaluation of protein intake by dietary diaries and urea-N excretion in children with chronic renal failure. European Study Group for Nutritional Treatment of Chronic Renal Failure in Childhood.

In 1988 a European multicentre, randomized trial was started in order to analyse the influence of protein intake on the progression of chronic renal failure in children. Compliance to the dietary prescriptions, i.e. protein intake, was checked by written dietary diaries and in addition by urinary urea-N excretion. This provided a unique chance to compare both methods in non-hospitalized children. Of a total of 200 patients 123 were selected, in whom at least 4 consecutive dietary diaries plus 4 completely collected 24-hour urine samples were available. Whereas urea-N excretion and simultaneously recorded protein intake did not correlate well, mean urinary urea-N excretion and mean protein intake of at least 4 observations in each patient correlated highly (r = 0.803, p = 0.0001). The difference between protein-N intake and urea-N excretion was not a constant amount of 0.031 g/kg/day as proposed by Maroni et al. [1985] but figured at 0.085 +/- 0.061 g/kg/day and was highly correlated to protein intake (r = 0.839, p = 0.0001). The correlation of protein intake and urea-N excretion was best described by the formula: protein-intake (g/kg/day) = (urea-N excretion [g/kg/day]x 15.39) -0.8 or protein intake (g/kg/day) = urea-N excretion (g/kg/day) x 9.5. Maroni's formula underestimated the high protein intake of young children. In only a few patients dietary diaries severely underestimated protein intake as compared to calculation by urea-N excretion.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1976

[Remarks on the use of shortened procedures in evaluating EDTA-induced urinary lead excretion].

Urinary lead excretion following EDTA administration was studied in 47 both normal and lead intoxicated subjects, mainly monitoring the rate of excretion through sequential urine samples. Urinary lead excretion patterns proved to be quite different in the examined subjects: in particular, great differences were noted in the onset of lead excretion increase. The six-hr lead excretion resulted to be 60,7% of the total 24-hr excretion, with, however, a very wide range (42% to 83%). Urine flow didn't appear to influence the rhythm of urinary lead excretion. There is sufficient evidence to justify the conclusion that evaluation of EDTA-induced urinary lead excretion on the basis of the first-six-hr results cannot be assumed as a reliable procedure, unless it is used for rough diagnostic screening purposes.

Edetic Acid↗
PubMed1993

Biliary copper excretion in acutely and chronically copper-loaded rats.

Biliary copper excretion was examined in rats with acute, continuous and chronic copper loads. Copper was excreted into bile, and the concentration peaked 40 min after a venous injection of copper sulfate (127 ng/gm body weight). The excretion was significantly inhibited by colchicine. Therefore some copper may be transported in hepatocytes by a vesicular pathway and excreted into bile. Biliary copper output increased over time and reached a plateau 180 min after a continuous venous infusion of copper sulfate (318 ng/gm body weight/hr) had started, when the concentration of copper in bile was much higher than that in plasma; the bile/plasma ratio of copper concentrations was 4.32 +/- 0.46. These data support the idea that copper transport involves a specific uptake and transport system. In chronically copper-loaded rats, hepatic copper content was significantly increased compared with controls, and reaction products for copper were observed in hepatocyte granules by light microscopic examination with p-dimethylaminobenzylidene rhodanine stain. The number of lysosomes in hepatocytes increased and the shape changed. In chronically copper-loaded rats the number of tubular lysosomes was very high. However, other organelles appeared to be normal. In these rats biliary excretion of not only copper but also acid phosphatase, a lysosomal enzyme, was significantly greater than the control. Therefore hepatocyte lysosomes may play an important role in biliary copper excretion. Furthermore, when biliary lysosomal excretion increases, the tubular lysosomes actively participate in this excretion.

Acid Phosphatase↗
PubMed1995

[Clearance, reabsorption and excretion of free and bound L-carnitine in children].

Acylcarnitines are by-products of fatty acid, pyruvate and some xenobiotics metabolism excreted in urine. We compare the renal handling of free and acylcarnitine in a group of 15 healthy children in relation to sodium and urea excretion and to sodium fractional tubular reabsorption (FTR%) and fractional excretion (FE%). Urea and sodium were determined by routine laboratory method; free and acylcarnitines by enzymatic one. FTR% and FE% were determined as a % of filtration load. Linear regression was used for calculation of correlation coefficient "r" from paired data. Low correlation (r = 0.25; p = 0.42) between urea and free carnitine excretion was observed; for excretion of acylcarnitine and urea correlation was much higher (r = 0.61; p < 0.03). Excretion of free correlation was negatively correlated with sodium FTR (r = -0.86; p < 0.001) and there was no correlation at all for acylcarnitine excretion and sodium FTR. It can be assumed:-neither excretion nor reabsorption of acylcarnitines are Na-dependent;-renal handling of free and total carnitines proceeds on different mechanisms.

Adolescent↗
PubMed1996

Pharmacokinetics of the new thyrotropin releasing hormone analogue montirelin hydrate. 1st communication: plasma concentrations, metabolism and excretion after a single intravenous administration to rats, dogs and monkeys.

The plasma concentrations, metabolism and excretion were studied in rats, dogs and monkeys after a single intravenous administration of 14C-montirelin hydrate (CAS 90243-66-6, 14C-NS-3). 1. The plasma concentration of radioactivity and the area under curve (AUC0-infinity) increased with the dose after intravenous administration of 0.25, 1 and 4 mg/kg to male rats. 2. Until 4 h after intravenous administration of 0.25 mg/kg, the plasma concentration of radioactivity decreased with half-lives of 0.512, 0.771 and 0.786 h in male rats, dogs and monkeys, respectively. The plasma concentration of radioactivity in rats increased 6-10 h after administration, suggesting enterohepatic circulation. 3. The plasma concentration of NS-3 in various animal species decreased biphasically after intravenous administration. The elimination half-lives, t1/2 beta, in rats, dogs and monkeys were 0.324, 0.679 and 0.682 h, respectively, and the steady state volumes of distribution, Vdss, were 0.248, 0.319 and 0.306 l/kg, respectively. 4. The binding of NS-3 to serum protein was less than 3% in rats, dogs, monkeys and humans. 5. Within 48 h after intravenous administration of 1 mg/kg to male rats, the excretion of radioactivity in urine, feces and expired air was 67.3, 15.0 and 14.8% of the dose, respectively (total 97.1%). The biliary excretion of radioactivity was 26.6% within 24 h after dosing. 6. No sex-related difference was found in plasma concentration of radioactivity or the excretion of radioactivity in urine, feces and expired air after intravenous administration of 1 mg/kg to male and female rats. 7. In male dogs, the excretion of radioactivity in urine and feces was 92.3 and 5.6% of the dose, respectively, during 72 h after intravenous administration of 0.25 mg/kg (total 97.9%). 8. In male monkeys, the excretion of radioactivity in urine and feces was 91.7 and 2.9% of the dose, respectively, during 72 h after intravenous administration of 0.25 mg/kg (total 94.6%). 9. The urinary excretion of NS-3 and its main metabolite CNK-6004 (deamidation product) during 24 h after intravenous administration was 31.4 and 25.3% of the dose in male rats, 45.4 and 30.1% in male dogs, and 20.2 and 48.0% in male monkeys, respectively. The biliary excretion of NS-3 and CNK-6004 in male rats was 1.1 and 17.4%, respectively, during 24 h after administration. 10. The radioactivity in the bile collected from donor rats that had received 14C-NS-3 was easily absorbed from the intestinal tract of recipient rats after intraduodenal administration of the donor's bile.

Animals↗
PubMed1996

Mechanism of the tissue distribution and biliary excretion of the cyclic peptide octreotide.

The hepatobiliary transport and tissue distribution of the cationic cyclooctapeptide octreotide were studies at steady state after its infusion, at various rates, in rats. After an increase in steady-state plasma concentration, marked decrease in the tissue to plasma concentration ratio was observed only in pancreas, the target organ of octreotide. A marked decrease in the biliary excretion clearance, defined with respect to the concentration in the liver, was also observed, suggesting that a transport carrier was involved in the biliary excretion. The plasma elimination and biliary excretion profiles of octreotide were determined in Eisai hyperbilirubinemic rats (EHBR), which have an hereditary defect of the active transport carrier for organic anions in bile canalicular membranes. Although biliary excretion of octreotide was significantly reduced in EHBR, compared with normal Sprague-Dawley rats, no difference was observed in biliary excretion clearance, defined with respect to the concentration in the liver, between Sprague-Dawley rats and EHBR. On the other hand, the liver to plasma concentration ratio in EHBR fell to half that in Sprague-Dawley rats. These results suggest that the decreased biliary excretion of octreotide in EHBR is due not to reduced biliary excretion ability but to reduced hepatic uptake of octreotide. We studied in vitro transport using bile canalicular membrane vesicles. A significant increase in the transport of octreotide by bile canalicular membrane vesicles was observed in the presence of ATP, and the estimated kinetic parameters K(m) and Vmax were 6.5 microM and 370 pmol/min/mg of protein, respectively. Similar ATP-dependent uptake was observed in bile canalicular membrane vesicles prepared from EHBR. We concluded that the biliary excretion of octreotide is by ATP-dependent primary active transport and that the carrier system for octreotide differs from the so-called "canalicular multispecific organic anion transporter," which is absent in EHBR.

Animals↗
PubMed1996

[Urinary oxalic acid excretion in chronic kidney failure and after kidney transplantation].

Urinary oxalic acid excretion was examined in 61 patients with chronic nephropathies and in 21 patients after renal transplantation with a varying mean glomerular filtration. In both groups of patients a correlation was found between the plasma oxalic acid and serum creatinine and by a hyperbolic correlation between plasma oxalic acid and creatinine clearance. Moreover the authors found a direct correlation between oxalic acid and FEoxalic acid and FE(Na)+, FEH20 and FE1-ascorbic acid in both patient groups. Various chronic nephropathies and treatment in both groups did not affect the revealed correlations. In 13 healthy subjects during the period of maximum water diuresis urinary Na+ excretion did not increase but there was a significant increase of the l-ascorbic acid and oxalic acid excretion. In a group of 8 patients in the polyuric stage of chronic renal failure without dialysis treatment under conditions of increased dietary NaCl intake (15 g/24 h) a significant increase of the urinary Na+ excretion was recorded while the l-ascorbic acid and oxalic acid excretion was unaltered. From the assembled values of the examined biochemical indicators ensues that urinary oxalic acid excretion, similarly as ascorbic acid excretion, depended on water excretion.

Adult↗
PubMed1979

Increased excretion of dimethyltryptamine and certain features of psychosis: a possible association.

The excretion of the hallucinogen dimethyltryptamine (DMT) and its precursor N-methyltryptamine (NMT) was studied among 74 recently admitted psychiatric patients and 19 normal persons. Both compounds were detected in 24-hour urine samples from all subjects. Dimethyltryptamine excretion was greatest in schizophrenia, mania, and "other psychosis" and tended to decline as clinical state improved. Psychotic depressives excreted smaller amounts of DMT more akin to those excreted by neurotic and normal subjects. Urinary NMT excretion was unrelated to psychiatric diagnosis. Ratings on the Present State Examination (PSE) also indicated that increased excretion of DMT was associated with psychotic rather than neurotic psychopathology. Forty-three percent of the variance in urinary DMT levels could be explained in terms of six of the 38 PSE syndromes. Syndromes suggesting elation, perceptual abnormalities, and difficulty in thinking and communicating were most correlated with raised urinary DMT excretion.

Adolescent↗
PubMed1996

Urinary glycosaminoglycan excretion in NIDDM subjects: its relationship to albuminura.

Nephropathy is a serious microvascular complication of diabetes mellitus which is preceded by a period of microalbuminura. Increased loss of proteoglycan (PG) from glomerular basement (GBM) has been postulated to alter glomerular charge selectivity which contributes to urinary loss of albumin. In this study we measured the excretion of urinary glycosaminoglycans (GAG), the degradation products of PG, in 82 non-insulin-dependent (NIDDM) (Type 2) diabetic and 34 non-diabetic subjects. We found that diabetic subjects had a significantly higher GAG urinary excretion rate compared to non-diabetic subjects (12.54 +/- 5.67 vs 8.80 +/- 3.99 micrograms glucuronic acid min-1, p = 0.0001). Categorizing for albuminuric status shows that the diabetic normo-, micro- and macroalbuminuric groups have a higher GAG excretion rate than non-diabetic subjects. Heparan sulphate (HS) GAG urinary excretion was measured in 25 samples from diabetic subjects and 18 non-diabetic subjects. Diabetic subjects excreted more HS GAG than controls both as a rate or as a percentage of total GAG (3.70 +/- 1.94 vs 2.38 +/- 1.48 micrograms glucosamine min-1, p = 0.02; 31.6% +/- 12.5 vs 23.1% +/- 10.4, p = 0.02). Categorizing for albuminuric status shows that micro- and macro-albuminuric groups have a significantly higher HS GAG excretion rate than non-diabetic subjects. We conclude that, as in IDDM, excretion of GAG and HS GAG is higher in NIDDM and may precede the development of microalbuminuria.

Age Factors↗
PubMed1992

Elevated sulfatide excretion in heterozygotes of metachromatic leukodystrophy: dependence on reduction of arylsulfatase A activity.

Sulfatide excretion in urine and arylsulfatase A (ASA) activity in leukocytes were determined in 10 homozygotes of metachromatic leukodystrophy (MLD), 7 obligate and 5 facultative MLD heterozygotes, 6 low ASA subjects (not related to MLD homozygotes), and in 9 controls. As compared to controls (sulfatides: 0-2 nmol/mg lipid; ASA: 101-287 nmol p-nitrocatechol/mg protein/hr), MLD homozygotes displayed highly increased sulfatide excretions (27-280 nmol) and low residual ASA activities (0-13 nmol). Of 12 MLD heterozygotes (ASA: 18-87 nmol) 10 showed increased sulfatides (3-24 nmol). All heterozygotes with ASA activity < 60 nmol (n = 8) had elevated sulfatide excretions (4-24 nmol). Thus, reduction of ASA activity below 40% of the mean value of controls seems to be the critical threshold for elevated sulfatide excretion in MLD heterozygotes. The low ASA subjects (ASA in the heterozygote range) excreted sulfatides in the control range, even those with ASA activities < 60 nmoles (n = 3; including a definite homozygote for ASA-pseudodeficiency; ASA:25 nmol). Statistical evaluation of sulfatide excretion and ASA activity in all subjects (n = 37) revealed a significant inverse relation (Spearman rank correlation; R = 0.8278, P < 0.001). The finding of elevated sulfatide excretion in certain MLD heterozygotes might point to increase of sulfatides also in the nervous system.

Adult↗
PubMed1992

Pre- and postweaning excretion of puberty-influencing chemosignals in house mice.

Pre- and postweaning excretion of urinary chemosignals that influence puberty in female house mice were tested. The dependent variable used to assess the effectiveness of urine samples collected from donor mice was the age of first vaginal estrus in young female mice. Preweaning excretion of the puberty-delaying chemosignal by females was affected by litter sex composition; this effect interacted with the age of the young donor females. In litters of all females, the substance occurred from about the age of 9 days and in litters with 6 females and 2 males the delay substance was released from about the age of 17 days. Grouping dams during gestation but not prior to conception resulted in excretion of the puberty-delaying substance in the female progeny from the age of 17 days or possibly earlier. Young male mice do not excrete the puberty-accelerating chemosignal prior to the age of puberty. However, giving young males injections of testosterone resulted in an earlier first excretion of the acceleratory signal, suggesting that the machinery for chemosignal production is operative prior to the time of sexual maturity. Caging young males with an adult female prior to puberty resulted in earlier excretion of the puberty-accelerating substance, while caging young males with adult males retarded excretion of the substance. The findings are discussed in terms of early hormone effects on behavior and with regard to consequences for the chemosignal systems in house mice.

Animals↗
PubMed1997

Nitric oxide donors stimulate bile flow and glutathione disulfide excretion independent of guanosine 3',5'-cyclic [corrected] monophosphate in the isolated perfused rat liver.

Nitric oxide (NO) modulates several metabolic functions in hepatocytes, but the role of NO in bile secretion has not been clearly defined. In the present study, we examined the effects of NO on bile flow and biliary HC03- and glutathione excretion in the isolated perfused rat liver and assessed the role of guanosine 3',5'-cyclic monophosphate (cGMP) in mediating these effects. The NO donors sodium nitroprusside (SNP) and S-nitroso-acetyl-penicillamine stimulated bile flow and increased both HCO3- and glutathione excretion. Increases in bile flow were linearly related to increases in biliary glutathione concentration and output (P < .0001), which were almost entirely caused by glutathione disulfide, whereas the excretion of reduced glutathione remained unchanged. NO donors increased cGMP concentrations in bile and perfusate, and the membrane-permeant cGMP analogue dibutyryl cGMP was also found to stimulate bile flow and HCO3- excretion. However, in contrast to the NO donors, dibutyryl cGMP did not increase glutathione excretion. Furthermore, the NO donors failed to stimulate bile flow in mutant TR- rats in which the canalicular transport of glutathione and glutathione conjugates is deficient, although dibutyryl cGMP increased bile flow and HCO3- excretion in the mutant rats as in normals. These findings indicate that exogenous sources of NO increase bile acid-independent bile flow by stimulating glutathione disulfide excretion, effects that are independent of cGMP.

Animals↗