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PubMed2000

High urinary catecholamine excretion predicts mortality and functional decline in high-functioning, community-dwelling older persons: MacArthur Studies of Successful Aging.

PURPOSE: Catecholamine release is a marker of stress, and high plasma norepinephrine levels have been associated with increased mortality. The predictive value of high urinary catecholamine excretion for functional decline and mortality in healthier older persons has not been determined. SUBJECTS AND METHODS: We used data from the MacArthur Studies of Successful Aging to determine the effects of high urinary catecholamine excretion on 3- and 7-year mortality and functional decline. In 1988, 765 high-functioning older subjects provided complete overnight urine samples for norepinephrine and epinephrine, and 199 of these provided repeat samples in 1991. Subjects who were in the top tertile of urinary norepinephrine or epinephrine excretion in 1988 were considered high excreters; those in the top tertile in both 1988 and 1991 were considered sustained high excreters. We used bivariate and multivariate analysis to examine the relations between high catecholamine excretion and mortality and Rosow-Breslau functional decline in 1991 and 1995. RESULTS: In multivariate analyses, subjects with high baseline urinary excretion of epinephrine, norepinephrine, or either catecholamine were at higher risk for mortality and functional decline at 3 and 7 years, although the magnitude of risk (adjusted odds-ratios ranged from 1.1 to 3.1) varied depending upon specific catecholamine and outcome measure. Subjects who had sustained high urinary norepinephrine excretion were also at increased risk for 4-year mortality or functional decline. CONCLUSIONS: High urinary catecholamine excretion in high-functioning, community-dwelling older persons likely reflects subclinical sympathetic stimulation and is a marker of increased risk for functional decline and mortality.

Aged↗
PubMedDate not supplied

Biological fate of sulfur mustard, 1,1'-thiobis(2-chloroethane). Urinary excretion profiles of hydrolysis products and beta-lyase metabolites of sulfur mustard after cutaneous application in rats.

The urinary excretion profiles of some metabolites of sulfur mustard were determined by gas chromatography/mass spectrometry after cutaneous application of sulfur mustard in rats. Excretion profiles of the individual metabolites thiodiglycol and thiodiglycol sulfoxide, derived from the hydrolysis of sulfur mustard, were determined in different groups of three rats. Concentrations of thiodiglycol detected increased up to 10 fold after treatment of the urine with hydrochloric acid, presumably because of the excretion of acid-labile esters of thiodiglycol. Free thiodiglycol, free plus esterified thiodiglycol, and thiodiglycol sulfoxide excreted over 8 days accounted for less than 0.3%, 1-1.5%, and 3.4-4.3%, respectively, of the applied dose of sulfur mustard. In a further study, a modified analytical method was applied to determine these hydrolysis products and their acid-labile esters as the single analyte thiodiglycol, after treatment with acidic titanium trichloride. The excretion profile of the combined hydrolysis products was compared with the excretion profile of a different group of metabolites of sulfur mustard derived from the glutathione/beta-lyase pathway. These were also reduced to a common analyte, 1,1'-sulfonylbis-[2-(methylthio)ethane], after similar treatment with titanium trichloride. Urinary excretion of hydrolysis products determined in 4 rats over 8 days accounted for 3.7-13.6% of an applied cutaneous dose of sulfur mustard. Urinary excretion of beta-lyase metabolites accounted for 2.5-5.3% of the applied dose in the same group of rats. The excretion of beta-lyase products showed a much sharper decline than was observed for the hydrolysis products of sulfur mustard.

Administration, Cutaneous↗
PubMed2001

Wheat bran and soy protein feeding do not alter urinary excretion of the isoflavan equol in premenopausal women.

The capacity to convert the soy isoflavone daidzein to equol in vivo is presumably determined by an individual's intestinal microfloral populations; however, diet may also influence this conversion. The objectives of the present study were to determine whether a 1-mo supplementation of dietary fiber as wheat bran increases urinary equol excretion in equol excreters and stimulates equol production in nonexcreters and whether longer-term soy isoflavone intake increases equol production or alters overall urinary isoflavone excretion. First, we screened 74 women, ages 20-40 y, and determined their equol-excreter status. In these women, health and lifestyle patterns and habitual dietary intake did not differ according to equol-excreter status. Next, 26 of the women (13 equol excreters and 13 nonexcreters) were assigned (blocked on equol-excreter status) to either longer-term (1 mo) or short-term (4 d) soy protein supplementation. Within each soy treatment group, women participated in two 1-mo intervention periods (the exact length was determined by each woman's menstrual cycle) during which they consumed their usual diets supplemented daily with either 0 or 16 g dietary fiber in a randomized crossover design. A 1-mo washout period separated the two diet periods. Among the 19 women who completed both periods, fiber supplementation did not increase equol production in equol excreters or nonexcreters. In addition, isoflavonoid excretion did not differ by fiber dose or length of soy intervention. These results suggest that a daily 16 g-fiber dose as wheat bran and the addition of soy protein do not alter significantly the capacity of colonic microflora to produce equol.

Adult↗
PubMed1998

Tranexamic acid, an inhibitor of plasminogen activation, reduces urinary collagen cross-link excretion in both experimental and rheumatoid arthritis.

The plasminogen activation system is one of the enzyme systems held responsible for bone and cartilage degradation in rheumatoid arthritis (RA). In this study, we evaluated the effect of tranexamic acid (TEA), an inhibitor of plasminogen activation, on urinary collagen cross-link excretion and radiological joint damage in rat adjuvant arthritis (AA) and on urinary collagen cross-link excretion in patients with RA. In the animal study, adjuvant arthritis was induced in male Lewis rats. From day 7 onward, high-dose TEA (500 mg/kg body weight, once daily) or placebo was administered orally. Study groups consisted of TEA-treated normal rats (C + TEA), placebo-treated normal rats (C + plac), AA rats treated with TEA (AA + TEA) or with placebo (AA + plac). To monitor joint destruction, urinary collagen cross-link excretion (pyridinoline, HP; deoxypyridinoline, LP) was measured by high-performance liquid chromatography at days 14 and 21. Radiological evaluation of joints was performed at day 21. In the patient study, TEA was administered to nine patients with RA as adjuvant medication (approximately 20 mg/kg body weight, three times daily) for 12 weeks. Urinary HP and LP excretion levels were measured before and during TEA treatment, and 4 weeks after the cessation of TEA treatment. In AA + TEA rats, a significant reduction of HP and a tendency towards a reduction of LP excretion were found compared with AA + plac rats (P < 0.05), at day 14, whereas the HP/LP ratio did not change. No difference was observed in HP, LP excretion, HP/LP ratio and radiological damage score between the TEA- and placebo-treated AA rats at day 21. In RA patients, a significant reduction of HP and LP excretion was found during the TEA treatment period (P < 0.05). After the cessation of TEA treatment, HP and LP excretion increased towards baseline levels. No effect on disease activity was observed. The plasmin antagonist TEA reduced the excretion of collagen pyridinoline cross-links in both experimental and rheumatoid arthritis. As such, this study not only supports the involvement of the plasminogen activation system in the destructive phase of arthritis, but also suggests a beneficial effect of therapeutic strategies directed against inhibition of matrix proteolysis.

Amino Acids↗
PubMed1990

Clinical study of urinary excretion of Ga-67.

Ga-67 urinary excretion was examined in 59 patients. The 72-hour urinary excretion rate ranged from 4.3 to 67.8% of the injected dose. Within the first 24 hours, 60.9% of the 72-hour urinary excretion was excreted. There was no significant difference in the Ga-67 urinary excretion rate between males and females, nor between the Ga-67 positive and negative cases. A significant negative correlation was found between the 72-hour Ga-67 urinary excretion rate and the unsaturated iron binding capacity. Notably, four patients with hyperferremia, which was considered secondary to leukemia and/or chemotherapy or liver cirrhosis, excreted more than 46.8% of Ga-67 within 72 hours. A significant negative correlation was also found between the 72-hour Ga-67 urinary excretion rate and age. Urinary excretion of Ga-67 may be related to the glomerular filtration rate, which decreases with age.

Adolescent↗
PubMed1989

Homeostatic regulation of potassium excretion.

Multiple systems participate in the homeostatic regulation of potassium excretion. Changes in plasma potassium, above a baseline value, will directly stimulate potassium excretion. Acute variations in aldosterone may have only small and perhaps insignificant effects in stimulating potassium excretion when aldosterone is present within its normal plasma range, but may be highly significant in determining the kaliuretic response to changes in plasma potassium or tubular flow rate. Elevation of plasma aldosterone to supraphysiological levels appears to produce increases in potassium excretion. Chronic variations in aldosterone are important, but not unique in determining renal potassium adaptation to chronic variations in potassium uptake. New lines of evidence point to sensors of potassium intake located in the hepatic portal vein or liver, or in enteric locations. A reflex control of potassium excretion, first demonstrated by Aizman and Finkenshtein et al. [120-123] in the dog, and independently suggested in a more general form for the sheep, may be integral in the regulation of potassium excretion in response to intake. With this feedforward control system, potassium excretion may be regulated without changes in systemic plasma potassium concentration. From diverse lines of investigation we find that there is a compelling argument for an important role for the brain in regulating both potassium excretion and its ICF/ECF ratio. One may speculate, albeit on the basis of preliminary information, that separate but analogous systems exist for sodium and for potassium, each involving the brain and each acting through specific humoral factors. For sodium, evidence is accumulating for a ouabain-like humoral agent, perhaps originating in the brain, which modulates renal sodium excretion and the sodium concentration of ICF. Both of these actions have been proposed to have an important influence on blood pressure regulation. The evidence presented here is compatible with a similar system for potassium. On the basis of these studies reviewed here, it is intriguing to speculate that an analogous humoral factor is involved in the regulation of potassium homoeostasis, and that its effects, when understood, may help to resolve current debates regarding the role of potassium in blood pressure regulation.

Aldosterone↗
PubMed1985

Pulmonary hydrogen and methane excretion following ingestion of an unabsorbable carbohydrate: a study of twins.

Pulmonary excretion of hydrogen and methane after administration of an unabsorbable disaccharide (lactulose) was determined in 228 adult Hungarian twins, 60 monozygous (MZ) and 54 dizygous (DZ) pairs. More than 98% of the subjects (224 of 228) excreted large amounts of hydrogen between 90 and 180 min after lactulose administration. Methane excretion in the fasting state was observed in 124 of 228 of the probands (54.4%), and 68 of 228 (29.8%) produced additional methane in response to lactulose ingestion. In contrast to hydrogen production, both methane excretion and production were significantly more frequent in females than in males. In the total group, and more distinctly in females, the correlation between peak hydrogen and methane concentrations was negative. Twin concordance of fasting methane excretion and lactulose-induced methane production was near 70% in both MZ and DZ pairs. Heritability estimates of methane excretion and production based on intrapair correlation and variance were smaller than unity, and intrapair correlation coefficients were larger in twin pairs living apart than in those living in the same household. Methane excretion is comparatively frequent in the Hungarian population, and a substantial proportion of fasting methane excreters (55%) produce additional methane from lactulose. The sex difference of methane excretion appears to be characteristic of European populations. The twin data disprove regular Mendelian inheritance of methane production and are suggestive of genetic effects in a multifactorial system.

Adult↗
PubMedDate not supplied

Relationship between breath and total body hydrogen excretion rates in neonates.

Our study examined the relationship of H2 excreted in breath to total body H2 excreted by neonates. We report simultaneously measured end-tidal H2 concentrations, plus breath H2 and total body H2 (breath H2 plus flatus H2) excretion rates in 10 neonates. End-tidal H2 concentrations varied from 2.4 to 192 ppm. Breath H2 excretion rates ranged from 0.20 to 6.5 and total body H2 excretion rates from 0.29 to 15.0 ml/h. The fractional breath H2 excretion in these infants was 48% (range 33-69%), compared with 21% reported in adults. The correlation coefficient for end-tidal derived H2 excretion and directly measured breath H2 excretion rates was 0.95 (p less than 0.001). We conclude that the proportion of total H2 excreted in the breath of neonates is increased compared with adults, suggesting that caution must be exercised when interpreting newborn breath H2 measurements and using adult norms.

Adult↗
PubMed2000

Cytomegalovirus urinary excretion and long term outcome in children with congenital cytomegalovirus infection. Congenital CMV Longitudinal Study Group.

BACKGROUND: Cytomegalovirus (CMV) is the most frequent cause of congenital infection, and both symptomatic and asymptomatic infants may have long term sequelae. Children with congenital CMV infection are chronically infected and excrete CMV in the urine for prolonged periods. However, the effect of prolonged viral replication on the long term outcome of these children is unknown. OBJECTIVE: To determine whether duration of CMV excretion is associated with outcome at 6 years of life in symptomatic and asymptomatic congenitally infected children. METHODS: Longitudinal cohort study. Children congenitally infected with CMV were identified at birth and followed prospectively in a study of long term effects of congenital CMV infection. The relationship between duration of CMV urinary excretion and growth, neurodevelopment and presence and progression of sensorineural hearing loss (SNHL) at 6 years of age was determined. RESULTS: There was no significant difference in the duration of viral urinary excretion between children born with asymptomatic (median, 4.55 years) and symptomatic (median, 2.97 years) congenital CMV infection (P = 0.11). Furthermore there was no association between long term growth or cognitive outcome and duration of viral excretion. However, a significantly greater proportion of children who excreted CMV for <4 years had SNHL and progressive SNHL compared with children with CMV excretion >4 years (P = 0.019, P = 0.009, respectively). CONCLUSIONS: Children congenitally infected with CMV are chronically infected for years, but the duration of CMV urinary excretion is not associated with abnormalities of growth, or neurodevelopmental deficits. However, SNHL and progressive SNHL were associated with a shorter duration of CMV excretion.

Adolescent↗
PubMed1998

Urinary excretion half-life of 11-nor-9-carboxy-delta9-tetrahydrocannabinol in humans.

The excretion of marijuana metabolites occurs over an extended period of time, yet few studies have been designed for accurate estimation of excretion half-lives. The authors monitored excretion of the primary urinary metabolite of marijuana, 11-nor-9-carboxy-delta9-tetrahydrocannabinol (THCCOOH), by gas chromatography-mass spectrometry in a controlled clinical study of marijuana smoking that included measurement of the drug in each urine void collected during the 3-week study. Terminal excretion half-lives of THCCOOH were determined in six healthy male subjects with histories of marijuana smoking; the study was conducted on the clinical research unit of a major medical institution. Subjects smoked a single marijuana cigarette (placebo, 1.75% or 3.55% THC) each week. Urine specimens (N=953) were analyzed under blind conditions for THCCOOH by gas chromatography-mass spectrometry. Mean+/-SEM half-lives calculated by the amount remaining to be excreted method after the low and high doses were 31.5+/-1.0 hours (range, 28.4 to 35.3 hours) and 28.6+/-1.5 hours (range, 24.9 to 34.5 hours), respectively, when a 7-day monitoring period was used. The amounts of THCCOOH excreted over a 7-day period were 93.9 +/-24.5 microg (range, 34.6 to 171.6 microg) and 197.4+/-33.6 microg after the low- and high-dose sessions. Longer half-lives, 44.3 to 59.9 hours, were obtained with a 14-day sample collection. This study documents the prolonged excretion of THCCOOH in urine and emphasizes the importance of study design in the precise estimation of terminal excretion half-lives. A sensitive analytical method and a prolonged specimen collection period are important study considerations in the monitoring of marijuana excretion.

Adult↗
PubMed1994

Urinary nitrate excretion is a noninvasive indicator of acute cardiac allograft rejection and nitric oxide production in the rat.

Cytokine induction of calcium-independent nitric oxide synthase is associated with production of large amounts of nitric oxide (NO). NO is a free radical that is rapidly degraded to nitrite and nitrate. Measurement of plasma and urinary nitrate is an indirect marker of NO production and previous studies have demonstrated that plasma nitrate rises with allograft rejection. The purpose of this study was to examine the temporal relationship between the rise in urinary nitrate excretion and the onset of graft rejection, and to determine the effect of conventional immunosuppression on nitrate excretion. The heterotropic model of cardiac transplantation in the rat was used, with Brown-Norway to Lewis allografts and Lewis to Lewis isograft controls. Twenty-four-hour urine specimens were collected before and after transplantation. Urinary nitrate excretion was measured by gas chromatography/mass spectrometry. Each group was treated with (1) no immunosuppression, (2) dexamethasone (3 mg/kg), or (3) CsA (10 mg/kg) on days 0, 1, and 2. Time to rejection for untreated allografts was 5.1 +/- 0.1 days, extending to 8.4 +/- 0.5 and 9.6 +/- 0.4 days with dexamethasone and CsA treatment, respectively. There was a significant rise in nitrate excretion on days 4, 7, and 9 for control, dexamethasone-treated, and CsA-treated allografts, respectively, preceding evidence of rejection. Untreated allograft rejection was associated with a peak in nitrate excretion 8 times that of basal excretion by isografts. Treatment of the allografts with dexamethasone and CsA significantly attenuated peak nitrate excretion compared with untreated allografts with a only a 2- to 3-fold rise preceding rejection. Results indicate that allograft rejection is associated with a dramatic increase in peak urinary nitrate excretion that is attenuated by standard immunosuppressive therapy. An increase in nitrate excretion precedes evidence of graft rejection, and may serve as a noninvasive marker of graft rejection.

Animals↗
PubMed2006

Fractional excretion of angiogenic factors in women with severe preeclampsia.

OBJECTIVE: We estimated the fractional excretions of soluble fms-like tyrosine kinase 1 (sFlt-1), vascular endothelial growth factor, and placental growth factor of severely preeclamptic women at the time of disease clinical manifestation. METHODS: Levels of free sFlt-1, vascular endothelial growth factor, and placental growth factor were measured by immunoassay from time-matched serum-urine samples from 64 women in the following groups: nonpregnant reproductive aged (n = 9), healthy pregnant controls (n = 13), mildly preeclamptic women (n = 15), and women with severe preeclampsia (n = 27). Urinary concentrations of angiogenic factors were normalized to creatinine and fractional excretions calculated. Correlations were estimated between fractional excretions of angiogenic factors, albuminuria, nonspecific proteinuria and urine protein-to-creatinine ratio. RESULTS: Severely preeclamptic women had more than double urinary vascular endothelial growth factor (P = .01) and fractional excretion of vascular endothelial growth factor compared with mildly preeclamptic women (P = .007) or pregnant controls (P < .001). Serum, urine and fractional excretion levels of sFlt-1 were much higher among severely preeclamptic women compared with all the other pregnant groups (P < .001). Conversely, severely preeclamptic women had lower serum placental growth factor levels compared with healthy pregnant women (P < .05) and mildly preeclamptic groups (P < .05). Severely preeclamptic women had increased fractional excretions of placental growth factor, albumin, proteinuria, and random urine total protein/creatinine ratio. Among severely preeclamptic women there was no correlation between proteinuria and fractional excretion of vascular endothelial growth factor (r = 0.30, P = .127) or sFlt-1 (r = 0.35, P = .07). There was a significant correlation between fractional excretion for placental growth factor, random urine total protein/creatinine ratio (r = 0.60, P = .002), and nonspecific proteinuria (r = 0.50, P = .01). CONCLUSION: Severe preeclampsia is characterized by increased fractional excretion of angiogenic factors and especially of vascular endothelial growth factor, likely reflecting 2 separate phenomena that may have additive effects: "endogenous" renal production and glomerular "leakage."

Adult↗
PubMed1982

Urinary excretion of prostaglandin F2 alpha and 6-keto-prostaglandin F1 alpha during volume expansion in patients with glomerulonephritis.

Thirteen patients with active IgA glomerulonephritis (IgA GN), ten patients with a history of Henoch-Schönlein glomerulonephritis (HS GN) and nine healthy controls were studied during hydropenia (HP) and 3% volume expansion (VE) with isotonic saline. Clearance of inulin and para-aminohippurate, urinary excretion of Na, immunoreactive prostaglandin F2 alpha (PGF2 alpha) and 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha) were determined. The patients with a history of HS GN had normal blood pressure and renal function. As in the controls, the urinary excretion of PGF 2 alpha decreased and the excretion of 6-keto-PGF1 alpha increased during VE. In the patients with IgA GN the glomerular filtration rate (GFR) was normal, markedly reduced and supernormal. Five patients had hypertension and an increased NA excretion in relation to the GFR during VE. As a group, the patients with IgA GN increased their urinary excretion of 6-keto-PGF1 alpha during VE, while the excretion of PGF2 alpha did not change. In relation to the GFR, the urinary excretion of PGF2 alpha and 6-keto-PGF1 alpha was markedly increased in two patients with low GFR, which implies that these substances play a role in advanced renal disease. VE had little effect on PG excretion in these patients. In the hypertensive patients the urinary excretion of PGF2 alpha and 6-keto-PGF1 alpha was the same as in those with normal blood pressure. PGs are therefore not likely to mediate the increased natriuretic response to VE in hypertension.

6-Ketoprostaglandin F1 alpha↗
PubMed1989

Urinary excretion of human epidermal growth factor in the various stages of diabetic nephropathy.

Epidermal growth factor (EGF) is a polypeptide mitogen first isolated from mouse submaxillary glands and later from human urine. We have examined the pattern of urinary excretion of human EGF (hEGF) in normal subjects and in diabetic patients with varying degrees of nephropathy. hEGF was measured by homologous radioimmunoassay and expressed in terms of urinary creatinine excretion. On the basis of their albumin excretion rate, the diabetic patients were divided into those with normoalbuminuria (albumin excretion rate 3.5 (1.4-9.8) micrograms/min; mean (range)), microalbuminuria (albumin excretion rate 75 (30-128) micrograms/min) and macroalbuminuria (289 (169-879) micrograms/min). The albumin excretion rate for the normal subjects was 3.7 (1.6-9.7) micrograms/min. The mean (range) hEGF excretion (nmol hEGF/mmol creatinine) was 0.69 (0.47-1.29) for 19 healthy subjects, 0.60 (0.16-1.36) for the normoalbuminuric group (n = 18; NS), 0.47 (0.10-0.83) for the microalbuminuric patients (n = 19; P less than 0.001 vs controls and normoalbuminuric diabetics) and 0.38 (0.10-0.63) for the macroalbuminuric group (n = 18; P less than 0.001 vs controls and normoalbuminuric diabetics). There was an inverse correlation between albumin excretion rate and hEGF: creatinine ratio (r = -0.49; P = 0.02). These results show a progressive decline in hEGF excretion in diabetic patients with varying degrees of nephropathy and do not support the hypothesis that increased kidney size seen in early nephropathy is due to excessive amounts of EGF in the urine.

Adult↗
PubMed1995

Urinary excretion of epidermal growth factor in living human kidney donors and their recipients.

Epidermal growth factor (EGF) is a growth-promoting peptide that is synthesized in the distal tubules of the kidney and excreted in urine. EGF has been suggested to play a role in the repair after renal tissue damage, as well as in compensatory growth of the remaining kidney after uninephrectomy. The present study examined the urinary EGF excretion after uninephrectomy and transplantation among relatives. The urinary EGF excretion rate and the glomerular filtration rate (GFR) were followed for 26-54 days in 16 healthy kidney donors and nine recipients. After uninephrectomy the median urinary EGF excretion rate in the donors was not 50% of the pre-operative value, but around 65% (95% confidence limits of the median on the fifth post-operative day: 59-72%). This suggests that there is a compensatory increase in the EGF excretion rate from the remaining kidney of around 30% after uninephrectomy. A similar compensatory increase was demonstrated for GFR, indicating that the compensatory changes in EGF excretion rate and GFR might be correlated. In the transplanted kidneys, GFR was consistently around 15% lower and EGF excretion rate around 40% lower than in the corresponding kidneys remaining in the donors. This might reflect ischaemic and drug-induced damage of the transplanted kidneys. The present study demonstrated a compensatory increase of around 30% in urinary EGF excretion from the remaining kidney after uninephrectomy in healthy humans. Whether EGF plays a role in the adaptive processes in the remaining kidney or whether changes in EGF excretion are merely of a secondary nature is still uncertain.

Adult↗
PubMed1982

The effect of ethacrynic acid, bumetanide, frusemide, spironolactone and ADH on electrolyte excretion in ponies.

The effect of ethacrynic acid, bumetanide, frusemide, spironolactone and anti-diuretic hormone (ADH) on the urinary and faecal excretion of water and electrolytes by ponies was studied. Ethacrynic acid, bumetanide, and frusemide given intravenously, increased urinary sodium excretion, and, excepting frusemide, decreased faecal sodium excretion. Given by stomach tube ethacrynic acid reduced urinary and faecal sodium. Bumetanide, given intravenously, spironolactone, frusemide and ADH increased urinary sodium and all except frusemide intravenously decreased faecal sodium regardless of route of administration. Ethacrynic acid and bumetanide, given by stomach tube or intravenously decreased urinary and faecal potassium excretion, as did spironolactone and frusemide given orally. Ethacrynic acid and bumetanide given orally or intravenously, frusemide given orally and ADH intranasally reduced urinary chloride excretion; these same drugs by the same routes also reduced faecal chloride excretion. Excepting frusemide given intravenously, and ethacrynic acid orally, the effect of the drugs studied was not the same on urinary sodium excretion as on faecal sodium excretion. This suggested that different mechanisms were involved in the control of sodium excretion by the kidney and in the gut. There were similarities in the treatment of potassium and chloride by these organs.

Animals↗
PubMed2004

Biliary excretion of azelnidipine, a calcium antagonist, in rats.

BACKGROUND AND AIMS: Azelnidipine (CS-905) is a novel dihydropyridine calcium antagonist that is known to be excreted in feces. To examine the mechanism of biliary excretion of azelnidipine, the authors studied its biliary excretion in Eisai hyperbilirubinuria rats (EHBR), multidrug resistance protein (Mrp)2-deficient rats, and the effect of cholephilic compounds on the biliary excretion of azelnidipine in rats. METHODS: Radiolabeled azelnidipine was intravenously administered to EHBR and control rats, and the biliary excretion of radiolabeled metabolites was studied. Furthermore, the effect of sulfobromophthalein, taurocholate and vinblastine on the biliary excretion of azelnidipine metabolites was also studied in control rats. RESULTS: The biliary excretion of azelnidipine metabolites was delayed in EHBR. The biliary excretion of azelnidipine metabolites was inhibited by sulfobromophthalein and vinblastine, but was not inhibited by taurocholate or phenothiazine pretreatment. CONCLUSION: These findings suggest that the metabolites of azelnidipine are excreted into the bile partly by Mrp2 and P-glycoprotein.

Animals↗
PubMed2004

Effects of colchicine on the maximum biliary excretion of cholephilic compounds in rats.

BACKGROUND AND AIM: Colchicine, an inhibitor of intracellular vesicular transport, has been reported to inhibit the biliary excretion of bile acids and organic anions, but the previous findings are controversial. In order to systematically evaluate the effect of colchicine on the biliary excretion of cholephilic compounds, we studied the effect of colchicine on the biliary excretion of substrates of various canalicular transporters, which were administered at or above the excretory maximum in rats. METHODS: Substrates of various canalicular adenosine triphosphate-binding-cassette transporters were infused at or above the rate of maximum excretion into rats, and the effect of colchicine (0.2 mg/100 g), which was intraperitoneally injected 3 h before, on the biliary excretion was studied. Furthermore, the effect of tauroursodeoxycholate (TUDC) co-infusion on the biliary excretion of taurocholate (TC) after colchicine treatment was also studied. RESULTS: The biliary excretion of TC and cholate administered at the rate of 1 micro mol/min/100 g was markedly inhibited by colchicine, whereas that of TUDC was not inhibited even with the infusion rate of 2 micro mol/min/100 g. TUDC co-infusion at the rate of 1 micro mol/min/100 g increased the biliary excretion of TC (1 micro mol/min/100 g), which was decreased by the colchicine pretreatment. The biliary excretory maximum of taurolithocholate-sulfate and sulfobromophthalein, substrates of the multidrug resistance protein 2, of erythromycin, a substrate of the P-glycoprotein, and of indocyanine green were not affected by colchicine. CONCLUSIONS: The different excretory maximums of TC and TUDC and the different effect of colchicine on the excretion of these bile acids are considered to be a result of different regulatory mechanisms of vesicular targeting of the bile salt export pump to the canalicular membrane by these bile acid conjugates. The vesicular targeting of the multidrug resistance protein 2 and the P-glycoprotein to the canalicular membrane is considered to be colchicine insensitive in the absence of bile acid coadministration.

ATP Binding Cassette Transporter, Subfamily B, Mem↗