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PubMed1987

An investigation into the neural regulation of calcium excretion by the rat kidney.

1. An investigation was undertaken to examine the action of the renal nerves on the reabsorption of calcium ions from the left kidney of sodium pentobarbitone anaesthetized rats. 2. Renal denervation had no effect on renal haemodynamics but increased urine flow, calcium excretion, absolute and fractional sodium excretions by 26% (P less than 0.02), 73% (P less than 0.02), 90% (P less than 0.001) and 82% (P less than 0.01), respectively, without affecting the calcium to sodium excretion ratio. In a group of animals which were similarly prepared but the renal nerves were not sectioned, neither renal blood flow, nor the excretion of water, calcium or sodium changed during the time course of the experiment although glomerular filtration rate increased significantly (P less than 0.05) by 19%. 3. Low rates (0.8-1.5 Hz at 15 V, 0.2 ms) of renal nerve stimulation did not change renal haemodynamics but reduced urine flow by 31% (P less than 0.001), calcium excretion by 32% (P less than 0.001), sodium excretion by 32% (P less than 0.001) and fractional sodium excretion by 32% (P less than 0.01) while the calcium to sodium excretion ratio was unaffected. Renal nerve stimulation at 3-5 Hz reduced renal blood flow by 15% (P less than 0.02), did not change glomerular filtration rate and reduced urine flow, calcium excretion, absolute and fractional sodium excretions by 35% (P less than 0.01), 30% (P less than 0.01), 32% (P less than 0.01) and 32% (P less than 0.05), respectively, while the calcium to sodium excretion ratio remained unchanged. 4. These data show that the renal nerves can modulate the excretion of calcium by a mechanism which is independent of renal haemodynamics and which may represent a direct action of the nerves on the calcium reabsorptive processes of the tubular cells. It remains to be determined whether this neural control of calcium reabsorption is a direct one or indirect via changes in sodium reabsorption.

Animals↗
PubMed1981

Renal nerves and catecholamine excretion.

To determine which neurotransmitters are released into urine by renal nerves, we either acutely denervated one kidney or stimulated renal nerves by activation of the baroreflex. Acute denervation increased dopamine (DA) and decreased norepinephrine (NE) excretion from the denervated kidney. In contrast, DA excretion decreased and NE excretion increased progressively from the contralateral innervated kidney. Sodium excretion related directly to DA and inversely to NE excretion. In chronic denervation experiments, baroreceptor stimulation increased NE excretion by 25% more from the innervated kidney than from its contralateral denervated mate, while DA excretion increased by 50% only from the innervated kidney. Baroreflex-stimulated NE and DA excretion from innervated kidneys was reduced by prior feeding of a low salt diet. The response was completely abolished by a high salt diet. Sodium excretion increased by the same proportion from innervated and chronically denervated kidneys following baroreceptor stimulation. In conclusion, 1) renal nerves release both NE and DA, 2) after acute unilateral denervation sodium excretion related directly with DA and inversely with NE excretion, and 3) urinary excretion of NE and DA derived from renal nerves was influenced by dietary sodium intake.

Animals↗
PubMed1999

Relationship between urinary calcium and net acid excretion as determined by dietary protein and potassium: a review.

Increasing urinary net acid (titratable acid + NH4 - HCO-3) excretion is accompanied by an increased urinary Ca excretion because of reduced renal tubular reabsorption of filtered Ca. The relationships between urinary Ca excretion rates and urinary net acid excretion rates are reviewed for data: (1) among healthy adults eating constant diets when net acid excretion is increased by increasing dietary protein, administering NH4Cl, or withdrawal of dietary KHCO3 or reduced by administering KHCO3; (2) among healthy adults eating constant diets providing varying amounts of protein and potassium, and (3) among healthy adults and Ca stone formers with and without idiopathic hypercalciuria eating ad libitum. The results show that urinary Ca excretion varies directly with net acid excretion by 0.035 mmol/mEq. The urinary net acid excretion increases by 0.10-0.15 mEq/mmol urinary urea, and urinary Ca increases by about 0.04 mmol/g dietary protein, while the urinary net acid excretion decreases as the ratio of urinary K/urea, a reflection of the dietary K relative to dietary protein, increases. The relationships between net acid excretion and both urinary urea and K/urea are similar among Ca stone formers without and with idiopathic hypercalciuria, but those with idiopathic hypercalciuria exhibit increased rates of urinary Ca excretion at all levels of net acid excretion.

Acids↗
PubMed2003

Calcium, sodium and potassium urinary excretion during the first five days of life in very preterm infants.

BACKGROUND: Hypercalciuria has been associated with the risk of nephrocalcinosis and renal stones in both adults and children. Renal calcifications are frequently encountered in preterm infants because this particular population presents most of the risk factors of increased urinary calcium excretion. Urinary calcium excretion has been shown to correlate with sodium and potassium excretions in adult patients, but these correlations have not been demonstrated in the early neonatal period yet. OBJECTIVE: To define the relationship between calcium urinary excretion and sodium or potassium excretions in the first 5 days of life in preterm babies. METHODS: A prospective study was conducted in 16 preterm infants born before 32 weeks of gestation (body weight 1,373 +/- 310 g; gestational age 29.1 +/- 1.6 weeks). Fifteen consecutive 8-hour urine collections were performed for each infant from the 8th hour of life. A plasma sample was obtained at the end of each urine collection. Sodium, potassium, calcium and creatinine were measured in urine and blood samples as often as possible. RESULTS: (1) Urine sodium excretion was 6.56 +/- 4.35 mmol/kg per day. (2) Urinary calcium excretion was 5.9 +/- 5.4 mg/kg per day and the urinary calcium/creatinine ratio was 0.48 +/- 0.39 mg/mg. (3) Urinary calcium and sodium excretion were positively correlated (r = 0.65, p = 0.0001), while an inverse correlation was found between calcium and potassium excretion (r = 0.31, p = 0.004). CONCLUSION: The mean values of urinary calcium excretion and calcium/creatinine ratio observed in our population were higher than 4 mg/kg per day and 0.4 mg/mg, respectively, i.e. boundary values previously associated with an increased risk of nephrocalcinosis. We hypothesize that an increase in urinary sodium excretion in this population may facilitate calcium excretion.

Birth Weight↗
PubMed1991

Urinary growth hormone excretion in 657 healthy children and adults: normal values, inter- and intraindividual variations.

Urinary growth hormone (u-GH) excretion was measured in 547 healthy children and 110 adults by ELISA with a detection limit of 1.1 ng/l u-GH after prior concentration of the urine samples (20- to 30-fold). u-GH excretion values were significantly dependent on the pubertal stage (p less than 0.0001) with maximum values in Tanner stage 3 for girls and 4 for boys. This corresponded to a peak in u-GH excretion between 11.5-14.5 years in girls and 12.5-16 years in boys. Additionally, u-GH excretion in adults was significantly higher than in prepubertal children (p less than 0.001). The day/night ratio of u-GH excretion (pg/h) was significantly higher in females than in males (p less than 0.01). In Tanner stages 1-4, u-GH excretion during the day was lower than that at night, whereas the opposite was true in late puberty and in adult women. The interindividual variation of u-GH excretion within the same Tanner stage was considerable and approximately double the intraindividual variation. The day-to-day variation could be further reduced by collection of three consecutive urine samples. The variations were larger if night samples instead of 24-hour samples were considered. The expression of u-GH excretion in nanograms per gram creatinine did not diminish the observed variation and blunted the pubertal increase in u-GH excretion. In conclusion, (1) u-GH excretion depends significantly on age, sex and pubertal maturation as does the day/night ratio of u-GH excretion. (2) The interindividual variation in u-GH excretion is considerable.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1996

Urinary growth hormone excretion in children and adolescents with insulin-dependent diabetes mellitus.

Urinary growth hormone (uGH) excretion was evaluated in 96 type-1 insulin-dependent diabetic patients and 37 age-matched healthy subjects. The growth hormone concentration was measured by a solid-phase immunoradiometric assay on 3 consecutive overnight urine collections. uGH excretion was comparable between diabetic patients and healthy subjects: 10.9 (0.1-34.8) vs. 9.1 (2.6-34.5) pg/min. In both groups uGH excretion was lower in prepubertal than in pubescent or pubertal individuals (diabetic patients, H = 29.7, p = 0.001; healthy subjects, H = 10.4, p = 0.006). In diabetic patients uGH excretion was related to beta 2-microglobulin excretion (r = 0.308; p = 0.005) and to urinary albumin excretion (r = 0.230; p = 0.02) but it was independent of HbA1c and overnight glycemic values. The coefficient of variation of uGH excretion was higher in diabetic patients with respect to healthy subjects: 50 (3-141) vs. 28(3-100)% (p = 0.002). Among diabetic patients it was greater in prepubertal than in pubescent or pubertal patients (H = 13.7; p = 0.002); in contrast, it was independent of pubertal stage in healthy individuals (H = 2.4; NS). The coefficient of variation of uGH was not related to HbA1c, the duration of diabetes, the coefficient of variation of urinary albumin excretion and the coefficient of variation of beta 2-microglobulin excretion. In conclusion uGH excretion is comparable among diabetic patients and healthy subjects, but its day-to-day fluctuation is greater in the former than in the latter group. Renal function but not metabolic control can influence uGH excretion. The day-to-day fluctuation in uGH excretion is independent of metabolic control and renal function.

Adolescent↗
PubMed1980

Urinary kallikrein excretion in essential and mineralocorticoid hypertension.

Urinary kallikrein excretion has been reported to be decreased in patients with essential hypertension and elevated in patients with primary aldosteronism as a reflection of mineralocorticoid activity. Low renin essential hypertension (LREH) has been postulated to result from excess production of an unknown mineralocorticoid(s). Urinary kallikrein excretion was compared in outpatients with essential hypertension, mineralocorticoid hypertension (primary aldosteronism and 17alpha-hydroxylase deficiency), and in normal subjects of the same race. No significant difference in urinary kallikrein excretion of patients with LREH vs. normal renin essential hypertension (NREH) was found for either black (4.1+/-0.4 vs. 4.8+/-0.5 esterase units (EU)/24 h, mean+/-SE, for 27 LREH and 38 NREH, respectively) or white patients (12.2+/-2.3 vs. 11.7+/-1.4 EU/24 h for 13 LREH and 25 NREH, respectively). Urinary kallikrein was decreased in black vs. white hypertensive patients and normal subjects. However, in patients with normal renal function (creatinine clearance >/=80 ml/min) urinary kallikrein was not significantly decreased in either black hypertensive vs. black normal subjects (4.3+/-0.3 vs. 5.4+/-0.6 EU/24 h) or in white hypertensive vs. white normal subjects (11.9+/-1.2 vs. 8.4+/-0.9 EU/24 h). In contrast, hypertensive patients with mild renal insufficiency (creatinine clearance of 41.8+/-78.5 ml/min) had reduced (P < 0.05) urinary kallikrein (3.3 EU/24 h with creatinine clearance of 63.6+/-2.0 for 24 black patients and 4.2+/-0.7 EU/24 h with creatinine clearance of 67.0+/-3.5 for 6 white patients). These results suggest that a reduction in urinary kallikrein excretion rate is an early accompaniment of hypertensive renal injury. Urinary kallikrein excretion in response to a 6-d 10-meq sodium diet and a 3-d Florinef (0.5 mg b.i.d.) administration was compared in hypertensive patients with normal renal function vs. race and age-matched normal subjects. Stimulation of urinary kallikrein excretion by Florinef was equal in black and white normal subjects vs. hypertensive patients (black normals = 12.3+/-2.7 [n = 9], NREH = 11.7+/-1.8 [n = 10], LREH = 10.9+/-1.5 [n = 12]; white normals = 21.2+/-2.9 [n = 11], essential hypertension = 20.9+/-3.2 [10 NREH, 5 LREH]). Stimulation of urinary kallikrein excretion with low sodium diet was decreased (P < 0.05) only in black LREH (black normals = 11.2+/-2.4 [n = 10], NREH = 10.1+/-2.7 [n = 10], LREH = 7.4+/-1.1 [n = 13]; white normals = 19.1+/-2.7 [n = 13], essential hypertension = 17.5+/-2.3 [nine NREH, four LREH]). However, during low sodium diet, black patients with LREH had evidence for less sodium depletion as manifested by a decreased rise in urinary aldosterone excretion (16.3+/-2.7 vs. 33.3+/-6.4 mug/24 h for black normals) and a failure to achieve metabolic balance in 11/13 patients. Thus, the lesser kallikrein stimulation appeared to result from these two factors. Black and white hypertensives with creatinine clearance <80 ml/min had little increase in urinary kallikrein excretion with Florinef or low sodium diet.5 of 12 patients with primary aldosteronism or 17alpha-hydroxylase deficiency did not have an elevated urinary kallikrein excretion rate. Mild renal insufficiency may have contributed to this finding in two of these five patients. Nevertheless, this finding illustrates a limitation to the use of urinary kallikrein excretion rate as an index of mineralocorticoid activity. However, it appears that the majority of patients with LREH have no evidence for excess production of an unknown mineralocorticoid. The failure to find a decrease in urinary kallikrein excretion in racially matched patients with essentil hypertension and normal renal function questions the postulate of a role of the kallikrein-kinin system in the initiation of essential hypertension.

Adult↗
PubMed1984

Role of vasopressin in regulation of renal kinin excretion in Long-Evans and diabetes insipidus rats.

To study the relationship between vasopressin and the renal kallikrein-kinin system we measured the rate of excretion of kinins into the urine of anesthetized rats during conditions of increased and decreased vasopressin level. The excretion of immunoreactive kinins in Brattleboro rats with hereditary diabetes insipidus (DI) (24 +/- 3 pg min-1 kg-1) was lower than in the control Long Evans (LE) rats (182 +/- 22 pg min-1 kg-1; P less than 0.05). The DI rats also exhibited negligible urinary excretion of immunoreactive vasopressin, reduced urine osmolality, and increased urine flow and kininogenase excretion. In LE rats, volume expansion by infusion of 0.45% NaCl-2.5% dextrose to lower vasopressin secretion reduced (P less than 0.05) kinin excretion, vasopressin excretion, and urine osmolality to 41, 26, and 15% of their respective control values, while increasing (P less than 0.05) urine flow and kininogenase excretion. On the other hand, the infusion of 5% NaCl, which promotes vasopressin secretion, increased (P less than 0.05) the urinary excretion of kinins and vasopressin to 165 and 396% of control, while increasing (P less than 0.05) urine flow and kininogenase excretion. Infusion of vasopressin (1.2 mU/h, intravenous) enhanced (P less than 0.05) kinin excretion by two to threefold in DI rats and in LE rats during volume expansion with 0.45% NaCl-2.5% dextrose, while decreasing urine flow and increasing urine osmolality. This study demonstrates that the urinary excretion of immunoreactive kinins varies in relation to the urinary level of vasopressin, irrespective of urine volume and osmolality and of the urinary excretions of sodium and kininogenase. The study suggests a role for vasopressin in promoting the activity of the renal kallikrein-kinin system in the rat.

Animals↗
PubMed1981

Renal cation excretion in the hypocalcemic premature human neonate.

We describe the interrelationship of the urinary excretion of sodium, calcium, magnesium, and phosphorus in 22 hypocalcemic premature neonates whose mean gestational age was 31.7 wk. Strong relationships between sodium excretion and calcium excretion (r = 0.85), sodium excretion and magnesium excretion (r = 0.76), sodium excretion and phosphorus excretion (r = 0.94) were demonstrated. Sodium intake during the 84-hr study period ranged from 2.9 to 34.5 mEq/kg and calcium intake during the same period ranged from 0 to 152.3 mg of elemental calcium per kg. The intakes of the other cations were negligible. All variables but phosphorus excretion (r = -0.55) were independent of calcium intake whereas sodium excretion (r = 0.76), calcium excretion (r = 0.72) magnesium excretion (r = 0.62), and phosphorus excretion (r = 0.53) were all correlated with sodium intake. Serum calcium concentration at the end of the study was unrelated to total calcium intake during the 84-hr study period, whereas it was negatively related to total sodium intake (r = -0.71).

Calcium↗
PubMed1987

The effect of tin (IV)-protoporphyrin-IX on bilirubin production and excretion in the rat.

Tin (IV)-protoporphyrin-IX alpha (tin-heme) may have use in treating neonatal jaundice. To evaluate its effect on bilirubin metabolism, we measured bile-bilirubin excretion in adult, male Sprague-Dawley rats (350-500 g). After a 4-h baseline period, tin-heme (100 mumol/kg) or buffer was injected subcutaneously, and bile was collected for 19 h. Bile flow, bile salt excretion, and bile-bilirubin excretion (averaging 600 +/- 60 ng/100 g/min for all animals) remained stable in the control period. Tin-heme treatment did not alter bile flow or bile salt excretion, but within 2 h bilirubin output was significantly reduced. The nadir of output was 5 h after injection when it was 380 +/- 40 ng/100 g/min (p less than 0.001). Cumulative excretion over 19 h was reduced 30.8% (p less than 0.01). To determine if tin-heme interfered with hepatic uptake or excretion of bilirubin, additional animals were administered intravenous bilirubin at 30 mg/kg/h for 3 h after tin-heme injection. Neither peak bile-bilirubin (37.4 +/- 4.68, control; 38.19 +/- 3.81 micrograms/100 g/min, treated) nor cumulative excretion (87.8 +/- 4.7, control; 88.9 +/- 4.2%, treated) were altered. Biliary excretion of tin-heme was measured under various experimental conditions. When administered alone, maximal excretion was 4 h after injection (4.41 +/- 1.58 micrograms/100 g/min); by 15 h, it fell to 0.024 +/- 0.011 microgram/100 g/min; 20-h cumulative tin-heme excretion in bile was 21.8 +/- 3.1% of the administered dose. Intravenous coadministration of albumin or albumin and bilirubin reduced the peak output but did not alter cumulative excretion of tin-heme. These data indicate that tin-heme reduces endogenous bilirubin formation but does not impair hepatic uptake and excretion. Bile is a major excretory route for tin-heme.

Animals↗
PubMed2004

Dogmas and controversies in the handling of nitrogenous wastes: the effect of feeding and fasting on the excretion of ammonia, urea and other nitrogenous waste products in rainbow trout.

Ammonia and urea are the primary forms of nitrogen excretion in teleost fish. There exists, however, a discrepancy between the sum of ammonia plus urea nitrogen and total nitrogen, indicating that 'unknown' nitrogen end products may play an important role in nitrogen metabolism. The current study analysed a wide range of nitrogen end products in both fed and fasted juvenile rainbow trout. Ammonia-N (53-68%) and urea-N (6-10%) were confirmed as the most important forms of nitrogenous waste, but an interesting finding was the considerable excretion of nitrogen as amino acids (4-10%), via the gills, and as protein (3-11%), probably via the body mucus. Use of anal sutures delineated an important role for the gastrointestinal tract in the production of ammonia-N and urea-N in fed fish, but amino acid-N and protein-N output by this route were both negligible. Alternative nitrogen products - trimethylamine, trimethylamine oxide, uric acid, and nitrite + nitrate - were not excreted in detectable quantities. Creatine-N and creatinine-N outputs were detected but contributed only a small fraction to total nitrogen excretion (<1.4%). Despite the wide scope of nitrogenous end products investigated, a considerable proportion (12-20%) of nitrogen excretion remains unknown. Possible alternative end products and methodological considerations are proposed to explain this phenomenon. The findings described above were used to recalculate the nitrogen quotient (NQ=(N)/(O(2))) on trout that had been either fasted or fed various daily rations (1%, 3% or 5% dry food per unit wet body mass per day). Feeding increased oxygen consumption ((O(2))) and total-N excretion ((N)). The NQ is often used as a measure of protein utilisation in aerobic metabolism and assumes that all protein (and amino acid) fuels are converted by oxidation to nitrogenous waste products that are excreted. However, the results showed that calculation of the NQ based on total nitrogen excretion may overestimate protein utilisation in aerobic metabolism because of significant excretion of N in the form of proteins and amino acids, whereas the use of summed ammonia-N and urea-N excretion probably underestimates the contribution of protein towards aerobic metabolism. These errors increase as ration increases, because the discrepancy between total-N excretion and ammonia-N + urea-N excretion increases.

Amino Acids↗
PubMed1995

Effects of feeding and confinement on nitrogen metabolism and excretion in the gulf toadfish Opsanus beta

In order to elucidate further the cues for, and the biochemical mechanisms of, the transition to ureogenesis in the gulf toadfish Opsanus beta, experiments on the effects of feeding (i.e. nitrogen loading) were carried out. Baseline nitrogen excretion rates were first measured on solitary toadfish in large water volumes (i.e. unconfined conditions). These nitrogen excretion rates were higher, and had a higher proportion as ammonia (61 %), than previously published 'control' measurements. Feeding of unconfined toadfish elevated total nitrogen excretion approximately threefold, with little change in the proportion of urea versus ammonia. During the first 24 h of confinement of unfed toadfish, absolute levels of urea excretion remained constant while ammonia excretion rates fell to near zero, so that toadfish became 90 % ureotelic. When fed prior to confinement, urea excretion rates remained constant for the first 24 h, and the bulk of the nitrogen was excreted as ammonia (80 %); excretion of the excess dietary nitrogen took up to 48 h to complete. If pre-adapted to confinement and then fed, toadfish excreted only about 55 % of their nitrogenous waste as ammonia, and excretion of excess dietary nitrogen was completed by 24 h. Elevations of hepatic glutamine synthetase (GNS) activities accompanied confinement and were shown to be almost exclusively in the cytosolic compartment and to be correlated with a decrease in the ratio of hepatic levels of glutamate:glutamine. These GNS activity increases also appear to account in part for the decrease in the percentage of ammoniotely in toadfish under conditions of nitrogen loading after confinement. However, additional means of regulating total nitrogen excretion (e.g. changes in protein turnover rates) and the degree of ureogenesis versus ammoniogenesis (e.g. N-acetylglutamate stimulation of carbamoylphosphate synthetase) must be postulated to account fully for changes in nitrogen excretion rates and activation of ureogenesis under some circumstances.

Journal Article↗
PubMed1975

An endocrine model for the diagnosis of intrauterine growth retardation as demonstrated by the determination of total estrogen and pregnandiol 24-hour urinary excretion in 222 at risk pregnancies.

A reliable method for surveillance of chronic impairment of nutritive placental function is described. The techniques are simple, tested for their reliability, without need for isotopes or special apparatus and hence inexpensive. Using 222 pregnancies at risk it is shown that the simultaneous determination of a fetal (estrogen) and a placental (pregnandiol) parameter makes the early diagnosis of intrauterine growth retardation possible. Estrogen diagnosis alone has a reliability of 90.1% with 1.8% falsely pathological and 8.1% falsely normal findings (Tab. I). Simultaneous pregnandiol determinations increase the number of falsely pathological findings to 8.1% but reduce that of falsely normal ones to 2.7%. No small for date (SGA) infants are found here. It consists of 5 cases of imminent (3 times actual) premature delivery and one postmature one. Hence our technique indicates the risk of intrauterine growth retardation in all cases but not the risk of premature or postmature delivery. Early diagnosis (from week 20) indicates that impairment of placental function as indicated by decreased pregnandiol excretion, occurs weeks or months earlier than decreased estrogen excretion (Fig. 1). This can be explained only by assuming that the rate of estrogen excretion is usually not dependent on the placenta but on the capacity of the fetal adrenals and liver. Thus our results indirectly confirm those of others who claim that the fetus can synthetize estrogen precursors without the need for placental pregnenolon by using acetate. Thus it appears that the synthetic pathway is independent of the placenta at the beginning plays a quantitative role also. Since the placenta can form aromatic compounds even when its nutritive function is severely impaired, our finding is further proof that estrogen excretion reflects fetal and not fetoplacental well-being. It follows that pathological estrogen excretion indicates fetal injury that has already occurred. The requirement that a sensitive parameter of placental function be hence determined in time is met by pregnandiol assays. Low pregnandiol excretion often precedes low estrogen excretion which leads to a SGA infant, indicating that pregnandiol excretion is closely correlated to placental nutritive function. Synthetic reactions in the fetus require energy and hence depend on the placenta. Normal estrogen excretion frequently observed in the presence of prolonged decreased pregnandiol excretion must hence indicate that the fetus can compensate for placental insufficiency. In the placenta this can be demonstrated by hyperplasia of the capillaries. This is reflected in the undulating excretion of pregnandiol (Fig. 1), where compensation (new vessel formation) and depression (lesion of vessels) make these contradictory placental processes "visible". The functional unity of the fetus and the placenta is finally also demonstrated by the fact that each prolonged compensatory phase of the placenta is reponded to by the fetus with a clearly compensatory excretion of estrogen (Fig. 1)...

Adult↗
PubMed1981

Effects of exercise on urinary excretion of albumin and beta 2-microglobulin in young patients with mild essential hypertension without treatment and during long-term propranolol treatment.

The effect of exercise on the urinary excretion of albumin, beta 2-microglobulin, renal plasma flow (RPF) and glomerular filtration rate (GFR) was studied in two groups of young patients with mild essential hypertension, one comprising nine untreated patients (1) and one comprising eight patients treated with propranolol (2), and in a group comprising ten normotensive healthy control subjects (3). The urinary excretion of albumin and beta 2-microglobulin, RPF and GFR were measured during four consecutive periods: a control period of 40 min; two exercise periods of 20 min each, with a load of 75 W and 100 W, respectively; and a control period. During exercise group 1 showed an increase in albumin excretion and a decrease in beta 2-microglobulin excretion, while group 2 showed an increase in albumin excretion during heavy exercise only and unchanged beta 2-microglobulin excretion, and group 3 showed unchanged albumin and beta 2-microglobulin excretion. RPF and GFR were reduced during exercise in all groups, most markedly in the hypertensive groups. During both exercise loads albumin excretion was higher and RPF was lower in group 1 than in 3. In group 2 albumin excretion was lower than in 1 during the light exercise load, whereas RPF and GFR were lower during both exercise loads. It is concluded that young patients with mild essential hypertension have both an abnormally high albumin excretion and an abnormally low RPF during exercise. During propranolol therapy urinary albumin excretion was partly normal. The changes in albumin excretion suggest glomerular leakage.

Adult↗
PubMed1978

Urinary oxalate excretion related to ileocolic surgery in patients with Crohn's disease.

Urinary oxalate excretion was studied in healthy subjects and before and after surgery in patients with Crohn's disease. Urinary oxalate excretion in relation to the length of diseased or resected ileal segment in patients subjected to restorative and colectomy procedures, as well as in relation to faecal excretion of fat and bile salts and to urinary excretion of vitamin B12 and calcium, was also studied. The studies were performed in patients on a free diet or standard hospital diet and on a high-oxalate and/or high-fat diet. When patients subjected to ileal resection in conjunction with minor colonic resection were studied on a high-oxalate diet, urinary oxalate excretion increased with length of ileum resected and correlated with faecal fat excretion and urinary excretion of vitamin B12 but not with faecal excretion of bile salts. Increasing the dietary fat intake in these patients further increased urinary oxalate excretion. Although urinary oxalate excretion increased somewhat in colectomized patients on a high-oxalate diet, indicating an increased absorption of dietary oxalate, this increase showed no correlation either to faecal fat or bile salt excretion, or to urinary excretion of vitamin B12. The result are consistent with the "solubility theory". A diet low in fat and oxalate and high in calcium is recommended in patients with hyperoxaluria.

Adult↗
PubMed1992

Urinary excretion of citrate, glycosaminoglycans, magnesium and zinc in relation to age and sex in normal subjects and in patients who form calcium stones.

One hundred and ninety-seven healthy subjects and 104 patients with idiopathic calcium stone disease had their urinary excretion of citrate, glycosaminoglycans, magnesium, and zinc measured and the results correlated with sex and age. In normal subjects the daily excretion of citrate, magnesium, and zinc increased with age to a maximum during the fifth decade and remained relatively constant until the eighth decade when they decreased. The daily excretion of magnesium and zinc were higher in men than in women, which was attributed to the higher body weights of the men. The urinary excretion of citrate, magnesium, and zinc related to creatinine remained relatively constant with age in adult life; analyses of magnesium and zinc excretion rates divided by urine creatinine did not distinguish men from women. There was no significant difference between men and women for citrate excretion in 24 hour urine, but the citrate:creatinine ratio was significantly higher in women than men. The higher citrate excretion in women may explain the lower incidence of calcium stones in women. The highest glycosaminoglycan excretion rates were seen during the first two decades which is why children and teenagers are less prone to develop calcium stones in spite of high urinary calcium concentrations. Urinary citrate and magnesium excretion were lower, and glycosaminoglycan and zinc excretion were higher, in stone formers than in controls. It seems that a decreased excretion of citrate and magnesium together with an increased excretion of calcium, may contribute to the formation of calcium stones. The role of urinary glycosaminoglycans and zinc in the formation of calcium stones remains uncertain.

Adolescent↗
PubMed2006

Prediction and evaluation of urine and urinary nitrogen and mineral excretion from dairy cattle.

Urine excretion is a substantial factor in the amount of manure that needs to be managed, and urinary N can contribute to ammonia volatilization. Development and validation of prediction equations focusing on dietary factors to decrease urine and urinary nutrient excretion will provide information for managing urine and feces separately or for other future technologies. The objective of this study was to develop equations for prediction of urine excretion and excretion of urinary N, Na, and K and to evaluate both new and previously published prediction equations for estimation of urine and urinary nutrient excretion from lactating dairy cows. Data sets from metabolism studies conducted at Washington State University were compiled and evaluated for excretion of minerals. Urine excretion averaged 24.1 kg/d and urinary nitrogen excretion ranged from 63 to 499 g/d in the calibration data set. Regression equations were developed to predict urine excretion, urinary N excretion, and urinary Na and K excretion. Predictors used in the regression equations included milk yield, body weight, dietary crude protein percentage, milk urea nitrogen, and nutrient intakes. Previously published prediction equations were evaluated using data sets from Washington State University and the University of Wisconsin. Mean and linear biases were evaluated by determining the regression of residuals on predicted values. Evaluation and validation of prediction equations are important to develop equations that will more accurately estimate urine and urinary nitrogen excretion from lactating dairy cows.

Animal Nutritional Physiological Phenomena↗
PubMed1983

The role of the adrenal gland in control of H+ and NH4+ excretion by toad urinary bladder.

The urinary bladder of Bufo marinus has been shown to excrete H+ and NH4+ and this excretion is increased by metabolic acidosis. The involvement of the adrenal gland and its steroid secretions in the adaptation for increased acid and ammonia excretion by the bladder was tested during the course of this study. Groups of toads were adrenalectomized and maintained in chronic NH4Cl-induced acidosis. Three other groups of toads were adrenalectomized and put in acidosis but repleted with 2.5 mg/day of either cortisol (CT), dexamethasone (Dexa), or deoxycorticosterone acetate (DOCA). All control groups were sham-operated. The bladders were excised after 3 days and mounted between 2-ml Lucite chambers. Net H+ and NH4+ fluxes into the mucosal media were measured and reported in units of nanomoles per 100 mg bladder per minute. In control acidotic toads H+ excretion was 20.1 +/- 2.0 and the adrenalectomized nonreplete group H+ excretion was 14.2 +/- 1.87 (P less than 0.04). For the same groups NH4+ excretion was 2.90 +/- 0.26 for the controls and 1.38 +/- 0.19 for the adrenalectomized (P less than 0.001). The H+ excretion in CT-, Dexa-, and DOCA-repleted toads was not significantly different from the control group. NH4+ excretion, however, showed a 55% decrease (P less than 0.001) in the CT group, and a 45% decrease (P less than 0.05) in the Dexa group. The NH4+ excretion in the DOCA repleted group was significantly different from the control group. Therefore, we conclude that the adrenal gland plays a role in the adaptive increase of H+ and NH4+ excretion by the urinary bladder in acidosis through the secretion of steroid hormones. The increase in NH4+ excretion appears to be a mineralocorticoid-stimulated process. We were not able to determine in this study if the steroid hormones had an exacting regulatory role or one of a permissive role over H+ and NH4+ excretion in the toad urinary bladder.

Acid-Base Equilibrium↗