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PubMedDate not supplied

The pharmacokinetics of hexachlorobenzene in male beagles. Distribution, excretion, and pharmacokinetic model.

The distribution of hexachlorobenzene (HCB) was studied in male beagles after a single 1-mg/kg iv dose of either 14C-HCB or unlabeled HCB. Distribution was also determined in animals after seven daily oral administrations of either 10 mg/kg or 100 mg/kg HCB. Excretion of HCB and metabolites through urinary and fecal routes was studied in all four animals receiving 14C-HCB. In addition, total bile was collected from one of the animals receiving 14C-HCB to determine the importance of biliary excretion. Immediately after iv administration, a large proportion of the dose was distributed to the lungs. From the lungs, HCB was rapidly distributed to highly perfused tissues including the visceral organs and brain. Further redistribution of HCB from highly perfused tissues to adipose tissue occurred at a much slower rate. In animals receiving daily oral doses of 10 or 100 mg of HCB per kg, adipose tissue was again found to accumulate the highest concentrations of HCB. Excretion of HCB and metabolites occurred primarily through fecal elimination, with urinary excretion being of less importance. Fecal excretion was found to be composed of two separate processes, biliary excretion and intestinal excretion. Of these two processes, biliary excretion was shown to be the major contributor to fecal excretion. After single 1-mg/kg IV doses of 14C-HCB in three beagles, blood, urine, and feces were monitored over a 12-week period for 14C content. Computer-assisted pharmacokinetic models were constructed to characterize these data. A three-compartment mammillary model provided the optimum fit to the observed data. Biological half-life values were projected to range from 6 weeks to 3 years.

Animals↗
PubMed1983

Depletion of hepatic uridine diphosphoglucuronic acid decreases the biliary excretion of drugs.

Hepatic levels of uridine diphosphoglucuronic acid (UDPGA) in rats decreased substantially (greater than 80%) 40 min after galactosamine (GAL) (600 mg/kg i.p.) or after 1 hr of diethyl ether (DE) narcosis. Biliary excretion of several cholephils requiring glucuronidation before excretion was reduced by GAL 76, 62, 92, 90 and 97% for bilirubin, diethylstilbestrol, iopanoic acid, phenolphthalein and valproic acid, respectively. GAL treatment caused delayed plasma clearances of the parent compounds and reductions in plasma concentrations and biliary excretions of glucuronide conjugates. The degree of this reduction was related to the maximal excretion rate of the individual compounds. For phenolphthalein glucuronide and phenol-3,6-dibromphthalein disulfonate, which do not undergo conjugation, GAL had no effect on their biliary excretion. DE-induced UDPGA depletion had no effect on phenolphthalein glucuronide excretion but reduced that of phenol-3,6-dibromphthalein disulfonate 25%. DE did not affect the plasma elimination or biliary secretion of phenolphthalein. Of the other cholephils requiring conjugation, DE reduced the excretion of bilirubin, diethylstilbestrol, iopanoic acid and valproic acid by 41, 29, 76 and 28%, respectively. DE decreased the plasma elimination of the parent compounds and the appearance of the conjugates in both plasma and bile. Reduction of glucuronide excretion into bile was less pronounced at higher doses of the cholephilic anions. Neither treatment reduced in vitro hepatic UDP-glucuronosyltransferase activity toward these substrates or substantially altered extrahepatic UDPGA concentrations. Thus, both GAL and DE decreased UDPGA to similar concentrations, but the biliary excretion of compounds requiring glucuronidation before secretion was depressed to a greater extent by GAL.

Animals↗
PubMed1983

Urinary excretion of renin in the dog: effect of changes in plasma renin.

By using standard clearance and stop flow techniques, studies were carried out in anesthetized dogs to clarify further the mechanism(s) of excretion of renin in urine. The clearance of renin was 0.61 +/- 0.19 ml/min in control experiments and increased significantly to 1.26 +/- 0.38 ml/min after furosemide. The fractional excretion of renin increased from 1.51 +/- 0.45% during control to 3.90 +/- 0.98% after furosemide. The rate of excretion of renin was increased 10-fold during furosemide diuresis associated with a 10-fold increase in plasma renin concentration. Extracellular fluid volume expansion also produced a diuresis but no increase in plasma renin or renin excretion. Hemorrhage produced a 3.5-fold increase in plasma renin concentration and a 200-fold increase in urinary excretion of renin. When renal artery perfusion pressure was reduced to one kidney, the excretion of renin in the urine from that kidney increased, whereas there was no significant change in the excretion from the contralateral kidney. Reduction in renal artery perfusion pressure was associated with a 3-fold increase in the concentration of renin in the renal vein from the experimental kidney but an insignificant 2-fold increase in the arterial plasma renin concentration. Stop-flow studies demonstrated that renin enters the urine with the glomerular filtrate. The decreased concentration of renin in samples from the proximal tubule suggests that renin is being metabolized and/or reabsorbed in this nephron segment. In the distal nephron, there appears to be a site in which renin may be added to the tubular fluid. The results of these studies suggest that renin excretion in the urine is a complicated process. Excretion of renin in the urine is related in part to plasma renin activity but probably more importantly to the rate of production of renin in the kidney.

Animals↗
PubMed1983

Biliary excretion of procollagen type III peptide in healthy humans and in patients with alcoholic cirrhosis of the liver.

Serum concentrations of procollagen type III peptide are found to be elevated in liver disease and to correlate with fibrosis activity in liver tissue. These elevated serum levels may be due to enhanced synthesis, decreased excretion, or release from deposits of the propeptide in connective tissue. To quantitatively investigate the excretion of procollagen type III peptide, we studied its presence in the bile and urine of 10 healthy controls and 11 patients with alcoholic cirrhosis of the liver. Biliary excretion rates of procollagen propeptide were determined by the duodenal perfusion method. The serum concentrations of procollagen type III peptide were 2.5 +/- 0.5 ng/ml in the healthy controls and 33.6 +/- 6.8 ng/ml in the patients with cirrhosis. Procollagen type III peptide was found in the bile; the healthy controls excreted 0.4 +/- 0.07 nmol/h and the cirrhotics excreted 0.98 +/- 0.27 nmol/h. A fragment of the procollagen propeptide, Col 1, was excreted in urine; the healthy controls excreted 0.25 +/- 0.04 nmol/h, and the cirrhotics excreted 0.11 +/- 0.03 nmol/h. These data demonstrate that the biliary excretion of procollagen type III peptide represents a quantitatively important pathway.

Bile↗
PubMed1982

Diurnal variation of urinary potassium excretion in chronic renal insufficiency.

Diurnal variation of urinary potassium excretion was examined on 10 adult patients with chronic renal insufficiency and 24 control subjects without cardiorenal functional disturbances. The daily cycle of potassium excretion, similar to that in controls, was present but less obvious in chronic renal insufficiency. In the controls, urinary potassium excretion reached a peak in the early morning (5.30 to 7.30) with a minimum in the night (21.00 to 5.30). The morning rise in potassium excretion was associated with increases in urinary sodium excretion, arterial blood pH, and plasma potassium and aldosterone concentrations. Creatinine clearance rate did not change significantly. In renal insufficiency, plasma potassium level and potassium excretion increased in the morning as compared with the night, whereas sodium excretion, the creatinine clearance rate, arterial blood pH and plasma aldosterone concentration did not change. 9 alpha-Fluorohydrocortisone gave rise to markedly enhanced potassium excretion. The findings suggest that the blunted cycle of potassium excretion in renal insufficiency is due, in part, to suppressed diurnal variations of sodium delivery to the distal tubule, acid-base balance and/or aldosterone secretion.

Adult↗
PubMed1980

Effect on renal sodium and water excretion of the inhibition of prostaglandin synthesis in extracellular volume expansion.

In anaesthetized dogs the effect of the inhibition of prostaglandin synthesis on renal function was investigated in isosmotic extracellular volume (ECV) expansion of 1.5-2% of the body weight. The degree of ECV expansion was then elevated to about 5% of the body weight by infusing intravenously 25 ml/kg of Ringer solution within 60 minutes. Arterial blood pressure, glomerular filtration rate, CPAH, water and sodium excretion, urinary osmotic activity and Evans blue distribution space were determined in mild ECV expansion and during and after Ringer load. Prostaglandin synthesis was inhibited by giving intravenously 4 mg/kg indomethacin in ten minutes. A group of animals, receiving no indomethacin only the solvent, served as control. Indomethacin induced first a fast and afterwards a slow continuous increase in arterial blood pressure. In the control group, arterial blood pressure did not change. Glomerular filtration rate was similar in both groups throughout the whole experiment. In mild ECV expansion indomethacin decreased the PAH clearance, and renal sodium and water excretion, and elevated urinary osmotic activity as compared to the control group. During an ECV expansion of about 5% of body weight, in the control group water excretion exceeded three-fold the initial value, while sodium excretion increased only by 50% and urinary osmotic activity decreased below that of the plasma. The Evans blue distribution space increased significantly. In the indomethacin-treated animals, urine excretion increased to double the initial value, sodium excretion was similar as in the control group, and urinary osmotic activity much higher than in the control group. The Evans blue distribution space was practically unaffected by the Ringer load. In the after-load periods, the parameters investigated came nearer to each other but there was still a marked difference between the control and the indomethacin treated group at the end of the experiment. Indomethacin reduced the increase of urinary excretion under the effect of ECV expansion; control animals excreted 42.8 +/- 11.6%, while the indomethacin-treated dogs excreted only 30.2 +/- 17.6% of the water load. The alteration in renal function observed under the effect of indomethacin is attributed to functional changes in different parts of the nephron, arising probably in consequence of changes in cortical and medullary blood flow.

Animals↗
PubMed1995

[Absorption, distribution, excretion and metabolism of [14C] T-3761 in rats and mice].

Absorption, distribution, excretion and metabolism were studied in rats and mice after oral and intravenous administration of 5 mg/kg of [14C] T-3761. 1. [14C] T-3761 was rapidly absorbed after oral administration and maximum serum concentration of radioactivity was observed at 15 min. and at 10 min. in rats and mice, respectively. After that, radioactivity of serum declined rapidly. 2. The administered radioactivity was excreted mainly in the urine in rats and mice and excretion rate was 84% and 74%, respectively. The residual radioactivity was excreted in the feces. In both species, the urinary excretion rate after oral administration was similar to that after intravenous administration, suggesting that [14C] T-3761 was absorbed almost completely. 3. In the rat urine, over 90% of excreted radioactivity was T-3761. On the other hand, about 57% of excreted radioactivity was presumed to be glucuronide conjugate of T-3761 in the mice urine. 4. The biliary excretion of radioactivity in rats after oral administration was approximately 22%, and about 83% of those was presumed to be glucuronide conjugate. About 40% of the excreted radioactivity was reabsorbed from the intestinal tract. 5. Except gastrointestinal tract, tissue concentration of radioactivity after oral administration was high in kidney and liver. Radioactivity was widely distributed in other tissues at lower concentration than in the plasma, whereas hardly distributed in brain and spinal cord. 6. Whole body autoradiograms in rats indicate that radioactivity were widely distributed except central nervous systems. 7. The extent of the binding of [14C] T-3761 to serum protein was 23-31% and 25-34% in rats and mice, respectively.

Administration, Oral↗
PubMed1993

Body composition, health status and urinary magnesium excretion among elderly people (Dutch Nutrition Surveillance System).

Magnesium (Mg) requirements depend on body weight. Recommended dietary allowances (RDA) are mostly given in absolute amounts and are mostly similar for adults, despite differences in body composition in the adult age range. We therefore studied the interrelations of 24 h urinary Mg excretion with body build and body composition indicators, as well as with factors potentially affecting the metabolism of Mg, among 520 elderly men and women seen in a nationwide survey. Mg intake data were also obtained in the Dutch Food Composition Survey amount 5898 subjects. The results showed lower mean Mg intake among elderly people (especially men) and positive associations of body weight and body height with urinary Mg excretion, but not when expressed per mmol of creatinine excreted. Mg excretion per mmol of creatinine was not associated with body weight, body height, body mass index or body fatness (women), suggesting that the amount of fat mass did not affect Mg excretion. Mg excretion was positively correlated with Mg intake, creatinine clearance, excretion of sodium, potassium and calcium, and coffee consumption, indicating interactions at the kidney level that may increase Mg losses. Elderly people using diuretics and/or anticholinergics and male diabetics had a higher mean Mg excretion per mmol of creatinine. The results show that, besides the Mg intake, several factors affect the urinary Mg excretion among elderly people. These factors were body build and body composition, dietary intake, drug use, kidney function, and diabetes. A quantification of the effects cannot be made yet, and controlled studies on those factors potentially affecting the requirement of Mg are needed.

Aged↗
PubMedDate not supplied

Effect of methadone dose on the biliary excretion of methadone metabolites in the rat.

The effect of three different doses of 14C-methadone (0.08, 1.0 and 2.5 mg/kg) on the biliary excretion of methadone metabolites was studied in the rat. After administration of the 0.08- and 1.0-mg/kg doses of 14C-methadone there was no difference in the percentage of administered 14C excreted into bile with time. However, after the 2.5-mg/kg dose a significant increase was observed in the percentage of administered 14C excreted into bile. Analysis of bile samples showed that this increase was due to increases in the biliary excretion of two of the major metabolites of methadone. Several mechanisms could be responsible for this disproportionate increase in biliary excretion of methadone metabolites after high doses of methadone. It was found that the effect of high methadone dose on the biliary excretion of its metabolites was nearly eliminated when studied in phenobarbital (PB)-pretreated rats. Pretreatment of rats with PB increases the biliary excretion of methadone metabolites, primarily by increasing rates of methadone metabolism. The lack of additivity of the effect of the high dose of methadone and PB pretreatment on the biliary excretion of methadone metabolites suggests that a high dose of methadone also stimulates methadone metabolism, which results in the observed increased percentage of the administered dose excreted into bile.

Animals↗
PubMed1996

Renal bicarbonate excretion in extremely low birth weight infants.

OBJECTIVE: To test the hypothesis that due to the immaturity of their kidneys extremely low birth weight infants lose large amounts of bicarbonate in their urine. METHODS: Urine and blood samples collected every 8 to 12 hours for the first 4 days of life from 22 preterm infants 23 to 29 weeks' gestation weighing 540 to 982 g at birth were prospectively studied. RESULTS: As described previously, three phases of fluid homeostasis were identified. The first phase (prediuresis) was a period of low urine output followed by a period of spontaneous diuresis/natriuresis (diuretic phase) and then by a phase when urine output varied according to fluid intake (postdiuresis). Sodium, potassium, chloride, and bicarbonate excretion rates and bicarbonate balance (bicarbonate or acetate infused minus bicarbonate excreted) were calculated for each of the three phases. Urinary excretion of sodium, potassium, chloride, and bicarbonate increased from the prediuretic to the diuretic phase and decreased from the diuretic to the postdiuretic phase. During the diuretic phase 88% of renal sodium excretion was accompanied by excretion of chloride. Bicarbonate balance was positive in all three fluid phases. Cumulative renal bicarbonate loss over the first 4 days of life was 1.9 +/- 0.5 meq/kg (SD) and the cumulative bicarbonate balance was +4.4 +/- 4.1 meq/kg (SD). The glomerular filtration rate, filtered load of bicarbonate, and absolute tubular reabsorption of bicarbonate significantly increased from the prediuretic to the diuretic phase, while fractional reabsorption of sodium and chloride decreased between these two phases. The fractional reabsorption of bicarbonate did not change from prediuresis to diuresis, but increased from diuresis to postdiuresis and consequently from prediuresis to postdiuresis. CONCLUSIONS: Contrary to our original hypothesis, the total renal bicarbonate excretion of extremely low birth weight infants in the first 4 days of life is low and the net bicarbonate balance is positive. The anion predominantly accompanying the excretion of sodium in all three phases is chloride and not bicarbonate. Bicarbonate excretion appears to be independent of sodium excretion during these phases. The increase in renal tubular bicarbonate reabsorption during the first week of life may be associated with extracellular volume contraction.

Bicarbonates↗
PubMed1996

Urinary NO3- excretion as an indicator of nitric oxide formation in vivo during oral administration of L-arginine or L-name in rats.

1. Endothelium-derived nitric oxide (NO), a major modulator of vascular tone, is synthesized from the terminal guanidino nitrogen of L-arginine. This reaction is inhibited by analogues of L-arginine, such as N-nitro-L-arginine methyl ester (L-NAME). Many of the biological effects of NO are mediated by the second messenger cGMP. NO is rapidly oxidized to NO3-, which, like cGMP, is eliminated via excretion into the urine. In a placebo controlled study, we investigated whether oral bolus administration of L-arginine and L-NAME affects the urinary excretion rates of NO3- and cGMP in Munich Wistar Frommter (MWF) rats. 2. Twenty MWF rats were kept in metabolic cages and received L-arginine (3 g/kg bodyweight), L-NAME (50 mg/kg), or placebo (0.9% saline) in randomized order. Urine samples were sequentially collected for 10 h and analysed for creatinine, NO3- and cGMP. 3. L-Arginine inducted a slight, but prolonged increase in urine flow, whereas L-NAME induced an early, transient increase in urine flow which was followed by a decrease. Creatinine clearance decreased by 65% after L-NAME, but was not affected by L-arginine or placebo. 4. Urinary NO3- and cGMP excretion rates transiently increased after L-arginine (NO3-: + 29%; cGMP: +16%) for 4-5 h, whereas L-NAME induced an immediate, pronounced and lasting inhibition of urinary NO3- and cGMP excretion (NO3-: -76%; cGMP: -46%). Urinary NO3- and cGMP excretions were significantly correlated (r = 0.755; P < 0.001). 5. Urinary excretion rates of NO3- and cGMP, expressed as mu mol/h, were correlated to urine flow (mL/h; r = 0.617 and 0.649, respectively; both P < 0.05), whereas after correction by urinary creatinine (mu mol/mmol creatinine) no correlation with urine flow was observed, indicating that these excretion rates were independent of renal excretory function. Thus we conclude that changes in the urinary excretion rates of NO3- and cGMP represent changes in NO production rates in vivo when expressed in relation to urinary creatinine. Urinary NO3- and cGMP excretion is modulated by acute NO synthase inhibition or substrate provision.

Animals↗
PubMed1997

Alteration in the biliary and urinary excretion of acetaminophen metabolites by nephrotoxicants in rats.

It has been shown that ureter ligation increases the biliary excretion of acetaminophen (AA) conjugates, mainly as the sulfate in rats. This study was conducted to examine the effect of nephrotoxicants-that induce renal damage without liver injury on the biliary and urinary excretion of AA metabolites. Renal damage was produced in male S.D. rats, 1 day after dosing with 200 mg/kg p.o. of hexachloro-1,3-butadiene (HCBD), or 3 day after the dosage of 7.5 mg/kg iv of cisplatin (CIS). Renal damage without liver injury was confirmed by measuring serum enzymes, creatinine and BUN levels. AA and its metabolites were measured for 3 hr by HPLC in rats injected iv with 150 mg/kg of AA. The excreted amounts of AA-glucuronide (AA-G), AA-sulfate (AA-S) and AA-glutathione into bile were reduced to 57, 18 and 73% of control rats, respectively, by HCBD. HCBD pretreatment also altered the urinary excretion of AA-G, AA-S and AA-mercapturate to 75, 14 and 118% of controls. CIS drastically reduced the urinary excretion of AA metabolites, whereas this compound significantly enhanced the biliary excretion of AA-S. However, CIS did not cause an increase in the percentage of the dose excreted as AA-G in bile. Both HCBD and CIS caused marked elevations in the blood concentrations of AA-G and AA-S. These findings suggest that: 1) not all renal malfunction results in increased biliary excretion of AA metabolites to compensate for the lack of renal elimination, and 2) the selective reduction in biliary and urinary excretion of AA-S by HCBD appears to occur by mechanism(s) other than through alteration of AA and its metabolites.

Acetaminophen↗
PubMed1976

Role of metabolism in the biliary excretion of methadone metabolites.

The biliary excretion of the major methadone metabolites was studied after the administration of purified 14C-labeled metabolites of methadone. The three methadone metabolites administered to rats were the pyrrolidine and pyrroline metabolites and the glucuronide conjugate of the hydroxylated pyrroline metabolite. We found that the excretion of 14C into bile was greater after administration of the metabolites which underwent fewer metabolic steps prior to biliary excretion. Phenobarbital pretreatment of rats increased the biliary excretion of 14C after the administration of the 14C-labeled pyrrolidine and pyrroline metabolites, both of which undergo further metabolism. Phenobarbital pretreatment did not change the biliary excretion of 14C-labeled glucuronide of the pyrroline metabolite which does not undergo further metabolism in the liver. Analysis of bile samples showed that the increased biliary excretion of 14C in phenobarbital-pretreated rats after administration of the labeled pyrrolidine and pyrroline metabolites was due primarily to increases in the biliary excretion of methadone metabolites which resulted from further in vivo metabolism of the injected metabolites. These data confirm our earlier suggestion (Roerig et al., Biochem. Pharmacol. 24: 355-362, 1975) that phenobarbital pretreatment increases biliary excretion of methadone metabolites by increasing hepatic metabolism of methadone. Furthermore, it can be concluded from these studies that metabolism is a rate-limiting process in the excretion of methadone metabolites in bile.

Animals↗
PubMed1976

Different inhibitory effects of 2,4-dinitrophenol, iodoacetate, and probenecid on renal excretion of p-aminohippurate, cyclopenthiazide, and sulfamethoxypyridazine in rats.

The present study was undertaken to determine whether the renal excretion of drugs can be modified by inhibition of the carrier system for organic acids in vivo. The renal excretion of p-aminohippurate is not influenced by 2,4-dinitrophenol but is reduced by iodoacetate and probenecid. The renal excretion of cyclopenthiazide is decreased by all inhibitors. Rats excrete only a very small portion of the administered dose of sulfamethoxypyridazine. Renal sulfamethoxypyridazine excretion is 3 times higher when the tubular reabsorption is blocked by simultaneous administration of NaHCO3. However, even then only a small portion of the injected dose is excreted. Renal sulfamethoxypyridazine excretion is only reduced by probenecid. This finding can be explained by the reduction of the urine volume. It can be concluded that p-aminohippurate and cyclopenthiazide are renally excreted by tubular secretion, whereas sulfamethoxy-pyridazine is excreted by glomerular filtration.

Aminohippuric Acids↗
PubMed1983

The hourly pattern of urine solute and electrolyte excretion following standard surgical trauma.

Although urine volume (and, less frequently, concentration) is often measured in the perioperative period, little attempt has been made to separate temporal phases of the intra- and postoperative response to surgery. In 7 patients undergoing standard severe single trauma and managed by a conventional regimen which included intraoperative Hartmann's solution, we have investigated the hourly pattern of urine solute and electrolyte excretion over the first 48 h. Contrary to expectation, in the first 5 h Na+ excretion increases in association with overall solute excretion, and thereafter progressively diminishes. K+ excretion increases 4 h postoperatively and remains elevated for 24 h, after which it returns to normal, even though Na+ excretion remains low. Free water excretion is negative for the first 24 h, though urine osmolality does not suggest a maximal antidiuretic response by the kidney--the highest concentration achieved being just below 800 mosmol/kg. In order to distinguish between the physiological adaptive changes due to starvation and those due to injury, the hourly pattern of urine solute and electrolyte excretion was further investigated in 12 healthy volunteers mimicking postoperative conditions. Apart from the early postoperative period, the hourly pattern of Na+, K+ and osmolar excretion shows no discernible difference from the operated group. These results show that, particularly in relation to Na+, the changes seen in the post-injury patient, even after major uncomplicated surgery, are largely adaptive, and this is especially striking at 24 h after surgery.

Esophagus↗
PubMed2006

Aquaporin-1 and aquaporin-2 urinary excretion in cirrhosis: Relationship with ascites and hepatorenal syndrome.

Several experimental models of cirrhosis have shown dysregulation of renal aquaporins in different phases of liver disease. We investigated the urinary excretion of both aquaporin-1 and aquaporin-2 in patients with cirrhosis at different stages of the disease. Twenty-four-hour urine was collected from 11 healthy volunteers, 13 patients with compensated cirrhosis (without ascites), and 20 patients with decompensated cirrhosis (11 with ascites without renal failure and 9 with hepatorenal syndrome). Aquaporin-1 and aquaporin-2 excretion was analyzed by immunoblotting. Urinary aquaporin-2 excretion was reduced in patients with cirrhosis compared to healthy subjects. A progressive decrease in urinary aquaporin-2 excretion was observed as the severity of cirrhosis increased, from compensated cirrhosis to cirrhosis with ascites and hepatorenal syndrome. Patients with hyponatremia had lower urinary aquaporin-2 excretion than patients without hyponatremia. Vasopressin plasma level did not correlate with aquaporin-2 excretion. There were no differences between healthy subjects and patients with cirrhosis with or without ascites in urinary excretion of aquaporin-1, but urinary aquaporin-1 excretion of those with hepatorenal syndrome was extremely low. In conclusion, patients with cirrhosis appear to exhibit a decreased abundance of renal aquaporin-2 and therefore lower water permeability in the collecting tubules. This may represent an adaptive renal response to sodium retention, with expansion of extracellular fluid volume and dilutional hyponatremia observed in those who have cirrhosis with ascites. Finally, aquaporin-1 does not appear to play a role in the progressive dysregulation of extracellular fluid volume in cirrhosis.

Aquaporin 1↗
PubMedDate not supplied

Hydrochlorothiazide-induced 131I excretion facilitated by salt and water.

Salt intake is restricted under clinical conditions for which thiazide diuretics are customarily used. Dietary iodide intake offsets any effect of thiazide on iodide loss. However, our correlation coefficients relating Na+ to Cl- to I- excretion indicate that as thiazide administration or sodium chloride intake increases renal Na+ and Cl- excretion, I- reabsorption by the nephron coordinately decreases. Increased sodium chloride and water intake by the dog doubled I-excretion rates. Hydrochlorothiazide increased the sodium chloride and water enhanced I-excretion rate as much as eight-fold. Without added NaCl, hydrochlorothiazide increased the excretion rate of 131I by three- to eightfold, acutely. Within five to seven days after 131I oral administration, hydrochlorothiazide (1 or 2 mg/kg twice daily) doubled the rate of 131I disappearance from plasma, reduced the fecal output of 131I, and increased its rate of renal excretion. When hydrochlorothiazide was administered, as much 131I was excreted in the first 24 hours as occurred in 48 hours when sodium chloride and water were given without hydrochlorothiazide. Thiazide administration in customary clinical dosage twice a day with substantial sodium chloride and water for the first two days after exposure to 131I, should therefore facilitate the safe excretion of 131I. This accelerated removal of 131I might be enhanced even more if thyroid uptake of 131I is blocked by administration of potassium iodide, as judged by the greater 131I recovery from thyroidectomized dogs.

Animals↗
PubMed1994

Evaluation of urinary pyridinium crosslink excretion as a marker of bone resorption in the rat.

The aim of this study was to evaluate the value of the urinary excretion of the pyridinium crosslinks, pyridinoline (Pyr) and deoxypyridinoline (D-Pyr), as markers of bone resorption in the rat. The excretion of the crosslinks was compared with that of urinary [3H]tetracycline ([3H]TC) excretion from chronically [3H]TC-prelabeled animals, a technique established to monitor bone resorption in the rat. Bone resorption was modulated by Ca restriction, infusion of PTH, thyroparathyroidectomy, and administration of different bisphosphonates. Furthermore, the urinary crosslinks were assessed in three different osteopetrotic mutations in the rat. We found a delayed response of Pyr and D-Pyr excretion to acute changes in bone resorption compared with [3H]TC excretion. This delay was 1 day after Ca restriction and longer after other treatments, such as PTH administration or bisphosphonate treatment, with which it was more than 3 weeks. In contrast, chronic states with stimulation or inhibition of bone resorption showed similar changes in excretion of the urinary crosslinks and [3H]TC, except after PTH administration. The excretion of the crosslinks was greatly reduced in osteopetrotic rats (op/op, tl/tl, and ia/ia) and increased to normal levels in tl/tl rats after stimulation of bone resorption by M-CSF administration. These results suggest that, in rats, urinary excretion of the pyridinium crosslinks reflects bone resorption in chronic but not always in acute conditions. The cause of this discrepancy is still unclear.

Amino Acids↗