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PubMed1985

Selective inhibition of renal thromboxane biosynthesis increased sodium excretion rate in normal and saline-loaded rats.

The excretion rates of renal thromboxane B2 (TXB2) and 6-ketoPGF1 alpha, the stable chemical metabolites of thromboxane A2 (TXA2) and prostaglandin I2 (PGI2) respectively, PGE2 and sodium were determined in normal and saline-loaded rats treated with the thromboxane synthetase inhibitor imidazole. In normal rats the administration of imidazole in doses which did not affect renal 6-keto-PGF1 alpha and PGE2 excretion but selectively inhibited renal TXB2 excretion, significantly increased the sodium excretion rate. Volume expansion with saline increased renal PGE2 and 6-ketoPGF1 alpha excretion but did not alter renal TXB2 excretion. The increase in renal prostaglandin excretion was accompanied by an increased sodium excretion rate. The administration of imidazole to saline-loaded animals also decreased renal TXB2 excretion but did not alter the increased excretion of renal PGE2 and 6-ketoPGF1 alpha. This reduction in renal thromboxane biosynthesis by imidazole further increased the sodium excretion rate. We suggest that TXA2 is a potent antinatriuretic factor as well as the most potent vasoconstrictor agent known.

6-Ketoprostaglandin F1 alpha↗
PubMed1989

Urinary kallikrein excretion during potassium chloride infusion in potassium-adapted rats: effect of amiloride.

1. Urinary kallikrein excretion in the anaesthetized rat was measured during intravenous KCl infusion in control and in K+-adapted rats. 2. The infusion of 0.1 mol/l KCl at 3.0 ml/h for 60 min in control rats resulted in a significant increase in urinary kallikrein excretion, associated with diuresis, natriuresis and kaliuresis. 3. When rats were offered 0.1 mol/l KCl to drink ad libitum for 14 days (K+-adaptation), the basal excretion of kallikrein was higher than in the control rats. In K+-adapted rats, intravenous infusion of 0.1 mol/l KCl resulted in significantly greater increase in urinary kallikrein excretion than in the control rats. 4. The Na+-channel blocker, amiloride (8.5 mg/kg body weight), significantly increased urinary kallikrein excretion immediately after injection in control and K+-adapted rats. However, in the subsequent 60 min, kallikrein excretion decreased markedly to values lower than those before injection of amiloride. 5. When amiloride was superimposed on a continuous 0.1 mol/l KCl infusion in K+-adapted rats, there was an immediate increase in kallikrein excretion. In the subsequent 20 min, kallikrein excretion decreased only to increase again in the next 40 min of KCl infusion. 6. Since amiloride injection reduces urinary kallikrein excretion in control and K+-adapted rats, the results suggest that urinary kallikrein excretion in the rat is through a mechanism(s) affected by amiloride. The high urinary kallikrein excretion and the greater response to KCl infusion in K+-adapted rats suggest that the K+-transport mechanism is more important than the mechanism affected by amiloride.

Amiloride↗
PubMed1992

Renal divalent cation excretion in secondary hypertension.

1. To determine whether abnormal renal calcium excretion is unique to primary genetic hypertension, blood pressure and 24 h urinary excretion of calcium, magnesium, sodium and creatinine were measured in deoxycorticosterone-saline and two-kidney, one-clip Goldblatt hypertensive rats and in their respective controls on low (0.2%) and high (1.8%) dietary calcium intakes. 2. Calcium supplementation lowered blood pressure (P < 0.05) in deoxycorticosterone-saline rats and in control saline-loaded rats, raised blood pressure in two-kidney, one clip rats, and had no effect in sham-operated control rats. 3. On both diets, calcium excretion was higher in hypertensive than in normotensive rats. The high calcium diet increased urinary calcium excretion in all rats, but the changes in urinary calcium excretion closely paralleled the diet-induced changes in blood pressure. Thus, urinary calcium excretion in deoxycorticosterone-saline animals, in whom calcium lowered blood pressure the most, rose the least (107%). Urinary calcium excretion rose the most in two-kidney, one-clip animals (1113%), whose blood pressure also rose the most. 4. Urinary magnesium excretion was also abnormal in hypertensive rats compared with normotensive rats, falling on the high compared with the low calcium diet in normotensive rats, but not in either hypertensive strain. Furthermore, urinary magnesium excretion was closely linked to urinary calcium excretion in saline-loaded control rats (r = 0.78; P = 0.008), but was dissociated from urinary calcium excretion in deoxycorticosterone-saline rats (r = 0.02; not significant).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1996

Biliary excretion of estradiol-17 beta-glucuronide in the rat.

Estradiol-17beta-glucuronide (E217G) is a cholestatic agent and is considered to be related to the pathogenesis of intrahepatic cholestasis of pregnancy. In the current study, we examined the mechanism of the biliary excretion of E217G and estradiol metabolites in rats. Biliary excretion of tracer doses of [3H]estradiol-17beta-glucuronide and [14C]estradiol or [3H]taurocholate and ]14C]vinblastine, a P-glycoprotein (P-GP) substrate, intravenously administered as a bolus to bile-drained control rats or EHBR was studied. Biliary excretion of E217G and estradiol metabolites EHBR was markedly delayed. Analyses of biliary metabolites after estradiol injection showed less polar conjugates in EHBR. In contrast, the excretion of taurocholate and vinblastine (VLB) was only slightly delayed in EHBR. Although phenothiazine treatment to induce the expression of P-GP increased biliary vinblastine excretion, it did not affect biliary excretion of a tracer dose of [3H]estradiol-17beta-glucuronide. However, phenothiazine treatment inhibited the cholestasis induced by E217G infused at the rate of 0.075 micromol/min/100g for 20 minutes and increased biliary E217G excretion. Sulfobromophthalein infusion (0.2 micromol/min/100 g body 0 weight) markedly inhibited the biliary excretion of E217G and estradiol metabolites, whereas dibromosulfophthalein (DBSP) at the same infusion rate had no effect. These findings indicate that EG17G is excreted into bile by a canalicular organic anion carrier for sulfobromopthalein (BSP), not for DBSP, under physiological conditions, and that P-GP influences E217G excretion only at a high dose. under physiological conditions, and that P-GP influence s E217G excretion only at a high dose.

ATP Binding Cassette Transporter, Subfamily B, Mem↗
PubMed2006

High urinary isoflavone excretion phenotype decreases plasma cholesterol in golden Syrian hamsters fed soy protein.

Apparent absorption of isoflavones varies greatly among individuals but is relatively stable within an individual. We hypothesized that high urinary isoflavone excreters would show less plasma non-HDL cholesterol (non-HDL-C) than low isoflavone excreters after soy protein feeding. Fifty Golden Syrian hamsters were fed a high-fat/casein diet (n = 10) or a high-fat/soy protein diet (n = 40) for 4 wk. We identified 2 distinct urinary isoflavone excretion phenotypes based upon HPLC analysis of urinary glycitein using a pairwise correlation plots analysis, or based upon total urinary isoflavone using a hierarchical cluster test. High isoflavone excreters showed greater urinary isoflavones (P < 0.05) than did low isoflavone excreters at wk 1 and 4. The low urinary glycitein excretion phenotype was more stable than the high urinary glycitein excretion phenotype by McNemar's test. High urinary isoflavone excreters had significantly less non-HDL-C than did the low isoflavone excreters or casein-fed controls (P < 0.05). Plasma total and non-HDL-C were negatively correlated with urinary daidzein, glycitein, and total isoflavone excretion (r = -0.45 to -0.58, P < 0.05). Urinary isoflavone excretion phenotypes predicted the cholesterol-lowering efficacy of soy protein. Isoflavone absorbability, probably due to gut microbial ecology, is an important controllable variable in studies of effects of soy protein on blood lipids.

Animals↗
PubMed2003

Lower urinary-interleukin-1 receptor-antagonist excretion in IgA nephropathy than in Henoch-Schönlein nephritis.

BACKGROUND: IgA nephropathy (IgAN) and Henoch-Schönlein nephritis (HSN) share many clinical, histological and immunological features. It has been postulated that these two conditions have a common pathogenesis and that HSN might be a systemic form of IgAN. Activity of interleukin-1beta (IL-1beta) in urine has been found to be higher in IgAN and HSN patients than in healthy controls. Interaction between IL-1beta and interleukin-1 receptor antagonist (IL-1ra) plays a significant role in the regulation of inflammatory responses. We studied levels of urinary excretion of IL-1beta and IL-1ra in patients with IgAN and HSN. METHODS: Amounts of IL-1beta and IL-1ra excreted in 24-h urine samples collected from 241 IgAN, 26 HSN patients and from 33 healthy controls were determined. Results were expressed as cytokine/creatinine (ng/mmol) ratios. RESULTS: Urinary IL-1beta excretion by the IgAN and HSN patients was no greater than urinary IL-1beta excretion by healthy controls. Urinary IL-1ra excretion by the IgAN patients was lower than urinary IL-1ra excretion by healthy controls (P < 0.05) and by the HSN patients (P < 0.01). In both patients and controls women had significantly higher IL-1ra, IL-1beta excretion levels and IL-1ra/IL-1beta ratios. The differences in urinary excretions of IL-1ra by the healthy controls and by the IgAN and HSN patients were significant in both sexes. Excretion of IL-1beta or IL-1ra did not correlate with excretion of urinary protein, duration of the disease or any histopathological variable. However, histopathological changes in renal biopsy specimens from patients with IL-1ra/IL-1beta ratios above normal were significantly milder than in renal biopsy specimens from patients with low or normal IL-1ra/IL-1beta ratios. CONCLUSION: Urinary IL-1ra levels in IgAN patients were lower than urinary IL-1ra levels in healthy controls or HSN patients, a finding which may indicate that the two diseases have a different pathogenesis. Whether the male predominance in IgAN and HSN and the worse outcomes in males that have been reported previously in IgAN and HSN are connected with the lower excretion of IL-1ra and consequently lower IL-1ra/IL-1beta ratios in male patients than in female patients needs more thorough investigation.

Adult↗
PubMed1989

Relationship between urinary kallikrein excretion and plasma atrial natriuretic factor in essential hypertensives.

Relationships between renal kallikrein and plasma atrial natriuretic factor were investigated by measuring urinary kallikrein excretion (by spectrophotometric assay) and plasma atrial natriuretic factor (by radio-immunoassay after extraction from plasma) in 84 normal subjects and in 104 essential hypertensives with a normal renal function. The atrial natriuretic factor was significantly higher in the essential hypertensives than in the normal subjects (38.5 +/- 1.3 versus 29.0 +/- 1.3 pg/ml, P less than 0.01), whereas urinary kallikrein excretion was significantly lower in the hypertensives than in the normal subjects (11.1 +/- 0.9 versus 15.3 +/- 0.6 nkat/24 h, P less than 0.01). Taking the 95% confidence limits of urinary kallikrein excretion in the normal subjects (from 4.5 to 29.9 nkat/24 h), we divided our essential hypertensives into two subgroups, patients with a normal kallikrein excretion (n = 80; mean urinary kallikrein excretion 13.8 +/- 0.8 nkat/24 h) and patients with a low kallikrein excretion (n = 24; mean urinary kallikrein excretion 2.3 +/- 0.3 nkat/24 h) The patients with a normal kallikrein excretion had a mean plasma atrial natriuretic factor value of 31.9 +/- 1.2 pg/ml, which was similar to that found in normal subjects. In contrast, the mean plasma level of atrial natriuretic factor in the patients with a low kallikrein excretion (50.7 +/- 2.2 pg/ml) was significantly higher than that measured in the patients with a normal kallikrein excretion and in the normal subjects (P less than 0.01 versus patients with normal kallikrein excretion and normal subjects, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)

Antibodies↗
PubMed1993

Aluminum Tolerance in Wheat (Triticum aestivum L.) (II. Aluminum-Stimulated Excretion of Malic Acid from Root Apices).

We investigated the role of organic acids in conferring Al tolerance in near-isogenic wheat (Triticum aestivum L.) lines differing in Al tolerance at the Al tolerance locus (Alt1). Addition of Al to nutrient solutions stimulated excretion of malic and succinic acids from roots of wheat seedlings, and Al-tolerant genotypes excreted 5- to 10-fold more malic acid than Al-sensitive genotypes. Malic acid excretion was detectable after 15 min of exposure to 200 [mu]M Al, and the amount excreted increased linearly over 24 h. The amount of malic acid excreted was dependent on the external Al concentration, and excretion was stimulated by as little as 10 [mu]M Al. Malic acid added to nutrient solutions was able to protect Al-sensitive seedlings from normally phytotoxic Al concentrations. Root apices (terminal 3-5 mm of root) were the primary source of the malic acid excreted. Root apices of Al-tolerant and Al-sensitive seedlings contained similar amounts of malic acid before and after a 2-h exposure to 200 [mu]M Al. During this treatment, Al-tolerant seedlings excreted about four times the total amount of malic acid initially present within root apices, indicating that continual synthesis of malic acid was occurring. Malic acid excretion was specifically stimulated by Al, and neither La, Fe, nor the absence of Pi was able to elicit this response. There was a consistent correlation of Al tolerance with high rates of malic acid excretion stimulated by Al in a population of seedlings segregating for Al tolerance. These data are consistent with the hypothesis that the Alt1 locus in wheat encodes an Al tolerance mechanism based on Al-stimulated excretion of malic acid.

Journal Article↗
PubMed1970

Excretion of Glycolate, Mesotartrate and Isocitrate Lactone by Synchronized Cultures of Ankistrodesmus braunii.

Fixation of (14)CO(2) by synchronized cultures of Ankistrodesmus braunii was highest for young growing cells, low for mature cells, and lowest for dividing cells. The amount of (14)C excreted during photosynthesis followed the same trend. Cells at the end of the growing phase, after 10 hours of a 16-hour light phase, excreted nearly 35% of the total (14)C fixed as one product, glycolate. Dividing cells from the dark phase, when tested in the light, excreted only 4% as much glycolate-(14)C as the young growing cells. Dividing cells also excreted as much mesotartrate as glycolate and also some isocitrate lactone and an unidentified acid. None of these excreted acids were found inside the cells in significant amounts. Methods for isolation and identification of the excreted acids are present. With (14)C-labeled algae, it was shown that the excretion of glycolate was light-dependent and inhibited by 1,1-dimethyl-3-(p-chlorophenyl) urea. The excretion of labeled mesotartrate, isocitrate lactone, and an unknown acid, but not glycolate, also occurred in the dark. The excreted mesotartrate was predominantly carboxyl-labeled even after long periods of (14)CO(2) fixation. Since glycolate is known to be uniformly labeled, glycolate could not be the precursor of the carboxyl-labeled mesotartrate. The reason for the specific excretion of glycolate, mesotartrate, and isocitrate lactone is not known, but the metabolism of all three acids by the algae may be limited and each can form dilactides or lactones by dehydration. In this context isocitrate lactone was excreted rather than the free acid.

Journal Article↗
PubMed1980

Increased urinary protein excretion after intravenous injection of furosemide in man.

The furosemide-induced increase in protein excretion, and its relations to 1) the size of protein molecules as reflected by three enzymes, and 2) glomerular filtration rate (GFR), plasma renin activity (PRA) and prostaglandin (PG) E2 and F2 alpha excretions were studied in 14 outpatients with normal renal function and 13 healthy males. Furosemide (120 mg) was given intravenously, and thereafter the protein excretion and the above parameters were monitored for 1--2 hours. In both groups, furosemide caused a transient increase in protein excretion. The excretion of the largest molecule, beta-glucuronidase, rose to 6.3-fold, while those of N-acetyl-beta-D-glucosaminidase and of the smallest molecule, alpha-amylase, increased by 91 and 37%, respectively. GFR increased, too, but markedly less than the protein excretion. PGE2 and PGF2 alpha excretions increased more than GFR and changed simultaneously with the excretion of proteins. Furosemide also caused a marked increase in PRA. This lasted, however, much longer than the rise in PG and protein excretion or GFR. The results suggest that the furosemide-induced increase in protein excretion is 1) related to the molecular size of proteins, 2) partly due to the rise in GFR, 3) simultaneous with the change in PG excretion. Our findings also agree with the view that furosemide causes changes in glomerular permeability.

Acetylglucosaminidase↗
PubMed1999

Attenuation by phenylbutazone of the renal effects and excretion of frusemide in horses.

The objectives of this study were to determine the effect of phenylbutazone premedication on the pharmacokinetics and urinary excretion of frusemide in horses; and on frusemide-induced changes in urinary electrolyte excretion. Six Standardbred mares were used in a 3-way crossover design. The pharmacokinetics and renal effects of frusemide (1 mg/kg bwt i.v.) were studied with and without phenylbutazone premedication (8.8 mg/kg bwt per os 24 h before, followed by 4.4 mg/kg bwt i.v. 30 min before frusemide administration). A control (saline) treatment was also studied. Administration of frusemide without phenylbutazone led to diuresis, natriuresis, kaliuresis and chloruresis, and altered the ratio of sodium:chloride excretion from 0.4 to 1.0 in the first hour of diuresis. When frusemide and phenylbutazone were administered, sodium and chloride excretion in the first hour were significantly (P<0.05) reduced by 40 and 32%, respectively, when compared to frusemide administrationwithout phenylbutazone. The fractional clearance of sodium and chloride was also significantly reduced. Potassium excretion, potassium fractional clearance and the ratio of sodium to chloride excretion were not affected by administration of phenylbutazone. During peak diuresis, phenylbutazone did not affect the efficiency of frusemide with respect to electrolyte excretion. The plasma disposition of frusemide was not affected by phenylbutazone. However, the renal excretion of frusemide decreased by approximately 25%. We conclude that the decreased urinary excretion of frusemide by phenylbutazone led to an attenuation of frusemide-induced increases in urinary excretion of sodium and chloride. Since the efficiency of frusemide was not affected by phenylbutazone, we conclude that phenylbutazone attenuates the renal excretion of frusemide without inhibiting the intrarenal activity of frusemide in horses.

Animals↗
PubMed1995

Lorry drivers' work stress evaluated by catecholamines excreted in urine.

OBJECTIVES: To evaluate lorry drivers' work stress by measurement of adrenaline and noradrenaline excreted in the urine, and to find out which factors in their working situation are related to the excretion rates of these catecholamines. METHODS: The urinary excretion of adrenaline and noradrenaline of 32 lorry drivers, who also had loading and unloading activities to perform, was studied for one working day and one rest day. Each driver was asked to provide six urine samples on both days. RESULTS: For all samples, except the first (overnight) sample, the excretion rates of both catecholamines on the working day were higher than those on the rest day. Hierarchical multiple regression analyses were carried out to find out which factors in the drivers' working situation were related to the excretion rate of the working day. The excretion rate of adrenaline on the rest day, age, and psychosomatic complaints were positively related to the excretion rate on the working day (all P < 0.05). Body mass index and physical workload during loading and unloading were positively related to noradrenaline excretion rate (both P < 0.01). Psychosocial job strain did not significantly contribute to the proportion of variance explained in the excretion rates of both catecholamines. CONCLUSIONS: The excretion rates of adrenaline and, especially, noradrenaline on the working day were higher than those found in earlier studies among professional drivers and insufficient recovery took place after the work was ended. The only association between excretion rate on the working day and work stressors was found for noradrenaline and physical workload. The drivers' sympathoadrenal medullary reactivity to everyday work demands shows the characteristics of sustained activation.

Adult↗
PubMed1982

Urinary excretion of acetylcarnitine during human diabetic and fasting ketosis.

The urinary excretion of acetylcarnitine was studied in patients with diabetic ketosis before and during insulin therapy and in normal-weight and obese subjects during fasting. In the diabetic ketotic patients, acetylcarnitine represented 61% of the total acylcarnitine excretion. During the first 24 h of insulin treatment, acetylcarnitine excretion decreased and on the 5th day of treatment was 18% of the acylcarnitines excreted. The urinary excretion of the other acylcarnitines fell slowly. In normal-weight subjects fasted for 3 days, the urinary excretion of acetylcarnitine increased on the 2nd day of fasting, and on the 3rd day acetylcarnitine accounted for 78% of the excreted acylcarnitine. In obese subjects there was a progressive increase in urinary acetylcarnitine excretion, but on day 6 it represented only 55% of the total acylcarnitine excreted. The urinary excretion of acetylcarnitine correlated with blood beta-hydroxybutyrate concentration in the normal-weight subjects during fasting and in the diabetic ketotic patients. Acetylcarnitine accounts for a major fraction of the acylcarnitines excreted in the three ketotic conditions studied. The contribution of acetylcarnitine to the change in acylcarnitines as ketosis appears or disappears is significantly less in the obese subjects than in the normal-weight subjects or in the diabetic patients. This difference may reflect an alteration in the production or disposition of acetyl-CoA and acetylcarnitine in obesity.

Acetylcarnitine↗
PubMed2001

Urinary prostaglandin D synthase (beta-trace) excretion increases in the early stage of diabetes mellitus.

OBJECTIVE: Circulating levels of lipocalin-type prostaglandin D synthase (L-PGDS)/beta-trace reportedly increase in renal failure as well as in cardiovascular injuries. We investigated the alterations of L-PGDS in urine and plasma in the early stage of type-2 diabetic patients. METHOD: Thirty-six type-2 diabetic patients and 29 normal subjects were studied. Overnight spot urine and plasma samples were obtained in the morning. L-PGDS was measured by ELISA method using anti-L-PGDS antibody. Variables indicating renal function were determined. RESULTS: Plasma L-PGDS concentration was slightly higher in the patients with diabetes mellitus than in the control subjects, whereas the urinary L-PGDS excretion almost doubled in the diabetic patients as compared with that in the control subjects. Plasma L-PGDS was determined by plasma creatinine (Cr) concentration while urinary L-PGDS excretion was correlated solely with urinary protein excretion. There was no relationship between plasma L-PGDS concentration and urinary L-PGDS excretion. The averaged plasma concentration of L-PGDS in the diabetics with a normal Cr level in plasma, corresponding to that in the controls, was determined by the plasma Cr concentration. On the other hand, the urinary L-PGDS excretion was determined by the amount of proteinuria and greater in the diabetics with a normal Cr level in plasma than in the controls even when the patients exhibited urinary protein excretion equal to that in the control subjects. CONCLUSIONS: Urinary L-PGDS excretion increased in the early stage of kidney injury in patients with type-2 diabetes mellitus. The urinary excretion was correlated independently with urinary protein excretion even when there was no difference in urinary protein or albumin excretions, thereby suggesting that urinary L-PGDS excretion is possibly a more sensitive indicator of renal injuries than proteinuria. Urinary L-PGDS may thus predict the progression of renal injuries in diabetic patients.

Analysis of Variance↗
PubMed2002

Increased urinary excretion of interleukin-17 in nephrotic patients.

BACKGROUND/AIM: Interleukin (IL)-17 is a newly discovered cytokine that is secreted by activated memory CD4+ T cells and modulated the early stage of immune response. To elucidate the pathophysiology of minimal-change nephrotic syndrome (MCNS), we focused on IL-17, which is one of the key factors in regulating an inflammatory response, and thus determined the daily excretion of IL-17 in urine. METHODS: For this purpose, excretion levels of IL-17 were measured in the urine of patients with MCNS during relapse and remission using a highly sensitive sandwich enzyme-linked immunosorbent assay. The data obtained were compared with levels of daily urinary excretion of IL-17 in patients with IgA nephropathy (IgAN). A group of healthy subjects served as control. In both experimental groups urine levels of IL-17 excretion were plotted against their daily urinary protein excretion. RESULTS: We demonstrated increased levels of IL-17 excretion in the urine of patients with MCNS and IgAN as compared to the non-nephrotic and healthy controls. In MCNS the daily urinary IL-17 (uIL-17) excretion was increased and returned to baseline with remission of the nephrotic syndrome (NS). We also demonstrated a positive correlation between urinary protein excretion and daily uIL-17 excretion. CONCLUSION: Taken together, these data indicate that uIL-17 excretion is increased during the NS, suggesting the possibility that daily uIL-17 excretion may reflect the disease activity of NS.

Adult↗
PubMed1992

Genetic influences on the urinary excretion of aldosterone in children.

Several studies have shown an inverse relation between blood pressure and plasma aldosterone levels. Since blood pressure is in part genetically regulated, we looked for evidence that genetic factors might also affect aldosterone production. The nocturnal urinary excretion rate was used to estimate aldosterone production, and electrolyte excretion rates were used to estimate sodium and potassium intakes. Studies were carried out in monozygotic (MZ) (n = 37 pairs) and dizygotic (DZ) (n = 26 pairs) twins, aged 6-17 years. Both groups of twins were white. The intraclass correlation coefficient for aldosterone excretion was 0.686 (p = 0.0001) for MZ twins, and 0.290 (p = 0.079) for DZ twins, indicating high heritability for the aldosterone excretion rate. In a second study, we looked for a racial effect on the genetic regulation of aldosterone excretion. Siblings from both black and white families (72 black siblings and 157 white siblings) were selected from an ongoing longitudinal study. Mean values for nocturnal aldosterone excretion, rates measured every 6 months over 1.5-3.5 years, were used in the analysis. The intraclass correlation coefficient for aldosterone excretion, adjusted for sodium and potassium excretion, was 0.510 (p = 0.001) for black siblings and 0.087 (p = 0.228) for white siblings, indicating a strong familial aggregation for aldosterone excretion in black children. In conclusion, studies in twins showed that regulation of urinary aldosterone excretion in children is determined partially by genetic factors. A familial component affecting the aldosterone excretion rate appears to be much stronger in blacks than in whites.

Aldosterone↗
PubMed1971

On the adaptation in potassium excretion associated with nephron reduction in the dog.

An effort to examine certain aspects of the adaptation in potassium excretion associated with nephron reduction was made in dogs with unilateral remnant kidneys. A constant intake of potassium was maintained by tube feeding and studies were performed before and after removal of the intact control kidney. The removal of the intact kidney created the need for the remaining nephrons of the remnant kidney to increase their rate of potassium excretion markedly. Sodium intake was held constant either at a normal or a low level. Mineralocorticoid hormone activity was maintained either at a high level by the administration of 0.2 mg 9-alpha-fluorohydrocortisone daily or at a low level by performing bilateral adrenalectomy and administering a minimal maintenance dose of deoxycorticosterone acetate (DOCA) and cortisol. Potassium excretion per nephron increased strikingly within 18 hr of contralateral nephrectomy and by 7 days, excretion rates were 600% of control values for the remnant kidney. More potassium was excreted in the first 5 hr after administration of a test dose of potassium by the remnant kidney alone in the postnephrectomy state than by both the remnant and intact kidneys in the prenephrectomy state. 24 hr excretion of potassium by the remnant kidney postnephrectomy averaged 92% of the administered load of potassium. The adaptation in potassium excretion was independent of the concurrent rate of sodium excretion and of mineralocorticoid hormone activity and persisted during constriction of the renal artery, a stimulus which presumably decreased distal delivery of sodium. The adaptation and the continued modulation of potassium excretion could not be explained adequately by an increase in impermeant anion excretion per nephron. Finally, known changes in hydrogen ion excretion per nephron associated with nephron reduction are in a direction opposite to those which would explain the acquired kaliuresis per nephron.

Adaptation, Physiological↗
PubMed1984

Urinary excretion of cadmium, protein, beta-2-microglobulin and glucose in individuals living in a cadmium-polluted area.

Urine was collected from 289 inhabitants of a cadmium-polluted quarter of Stadskanaal. The excretion of cadmium, protein, beta-2-microglobulin and glucose were determined. After being divided according to sex and to smoking habits, the results of the inhabitants were compared with those of 293 controls. In inhabitants as well as controls, cadmium excretion was age-dependent. Cadmium excretion in females increased faster with age than in males. In male-smoker controls, cadmium excretion was significantly higher (p less than 0.001) than in male-non-smoker controls. In male-non-smoker inhabitants, cadmium excretion (p = 0.05), protein excretion (p less than 0.01) and glucose excretion (p less than 0.01) were significantly higher than in corresponding controls. In male-smoker inhabitants, protein excretion (p less than 0.01) and glucose excretion (0.01 less than p less than 0.05) were significantly higher than in corresponding controls. In female-non-smoker inhabitants glucose excretion was significantly higher (0.01 less than p less than 0.05) than in corresponding controls. For some categories, living in the polluted area was associated with an increased cadmium excretion in urine and a slight difference in renal function, possibly related to a difference in cadmium body burden. It was concluded that, considering the actual values of each parameter, the observed differences were not relevant in terms of potential health hazards.

Adolescent↗