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PubMed1994

Altered urinary porphyrin excretion in a human population chronically exposed to arsenic in Mexico.

1. A detailed study of the urinary excretion pattern of porphyrins in humans chronically exposed to As via drinking water was performed using high performance liquid chromatography (HPLC) 2. Thirty-six individuals (15 men and 21 women) were selected from a town which had 0.400 mg L-1 of As in drinking water. The control group consisted of thirty-one individuals (13 men and 18 women) whose As concentration in drinking water was 0.020 mg L-1. 3. The major abnormalities in the urinary porphyrin excretion pattern observed in arsenic-exposed individuals were: (a) significant reductions in coproporphyrin III excretion resulting in decreases in the COPRO III/COPRO I ratio, and (b) significant increases in uroporphyrin excretion. Both alterations were responsible for the decrease in the COPRO/URO ratio. 4. No porphyrinogenic response was found in individuals with urinary As concentrations below 1,000 micrograms of As g-1 of creatinine. However, as arsenic concentrations exceeded this value, the excretion of porphyrins (except coproporphyrin III) increased proportionally. 5. The prevalence of clinical signs of arsenicism showed a direct relationship to both As concentration in urine and time-weighted exposure to As. A direct relationship between time-weighted exposure and alterations in urinary porphyrin excretion ratios was also observed. 6. The alterations found are compatible with a lower uroporphyrinogen decarboxylase activity in arsenic-exposed individuals. However, the similarities in the urinary porphyrin excretion pattern between As-exposed individuals and Dubin-Johnson syndrome patients suggest that impairments in the excretion of coproporphyrin isomers may also contribute to the pattern observed.

Adult↗
PubMed1986

Urinary arginine vasopressin: pattern of excretion in the neonatal period.

The pattern of arginine vasopressin (AVP) secretion in the immediate neonatal period is unclear. Plasma concentrations of AVP are reflected by its urinary excretion, thus providing a noninvasive method for studying the pattern of AVP release in the neonate. In these studies, we determined the pattern of urinary AVP excretion (microU/mg creatinine) during the first 2-4 days after birth in 78 neonates, 53 of whom had various prenatal and/or neonatal complications. In well term (n = 12) and preterm (n = 13) infants mean urinary AVP excretion decreased gradually during the first 24-36 h after birth. Although term and preterm infants with perinatal asphyxia had highest initial levels of urinary AVP (greater than 200 microU/mg creatinine) and a significant negative correlation with the 1-min Apgar score was obtained, their pattern of excretion was similar to respective controls. After delivery, elevated values for urinary AVP excretion were found among infants with neonatal courses complicated by intracranial hemorrhage, hypoxic encephalopathy, and pneumothorax. Urine osmolality did not correlate linearly with urinary AVP levels, but rather attained a maximum value of approximately 400 mosmol/kg at urinary AVP levels less than 200 microU/mg creatinine and then plateaued. It is concluded that the decrease in urinary AVP excretion observed soon after birth generally reflects diminution of the hypersecretion of AVP during parturition; neonates with evidence of intrapartum asphyxia initially have increased urinary AVP excretion; however, the pattern of excretion is similar to normal infants. During the neonatal period insults such as pneumothorax and intracranial hemorrhage may cause hypersecretion of this hormone.

Amniotic Fluid↗
PubMed1987

Fecal and urinary excretion of six iodothyronines in the rat.

Fecal and urinary excretion rates of six iodothyronines were assessed in the rat maintained under normal steady state physiological conditions, to gain a more comprehensive understanding of the mechanisms of control of normal thyroid hormone economy and metabolism. Groups of young adult male rats were injected with trace doses of T4, T3, rT3, 3,3'-diiodothyronine (T2), 3',5'-T2, or 3'-monoiodothyronine, each labeled with 125I, and feces and urine were collected separately for up to 10 days. Pooled fecal pellets were homogenized in saline, extracted in ethanol, evaporated under vacuum, and reconstituted in NaOH. Fecal extracts and urine were chromatographed on Sephadex G25 columns under conditions providing quantitative separations of components of interest. A new technique was also developed, based on a model of the in vitro extraction and measurement process, to correct chromatographic results for possible variable recoveries and possible artifactious degradation of radioactively labeled components. No iodothyronines or their conjugates were excreted in urine; all radioactivity was in the form of iodide. In feces, about 30% of the [125I]T3 injected was excreted as T3; and 24% of the [125I]T4 injected was excreted as T4, plus 4% as T3. Together, these results imply that about 24% of endogenous T4 production is excreted as T4 and 76% is irreversibly metabolized; and for T3, about 30% of endogenous T3 production is excreted as T3 and 70% is degraded. For the nonhormonal iodothyronines, about 6% of injected monoiodothyronine, 3% of injected 3',5'-T2, 2% of injected 3,3'-T2, and less than 1% of injected rT3 were excreted in feces as such, indicating that these substances are nearly completely deiodinated in vivo. Very little (1-7%) iodide was excreted as such in feces, which also were devoid of measurable conjugates. An open question is whether the substantial wastage of thyroid hormones in feces represents poor hormone economy in the usually accepted sense or a functional property of overall thyroid hormone regulation.

Animals↗
PubMed1988

19-Nordeoxycorticosterone excretion in male and female inbred salt-sensitive (S/JR) and salt-resistant (R/JR) Dahl rats.

Rats were selectively bred for susceptibility (S) and resistance (R) to the hypertensinogenic effects of excess salt intake by Dahl and further inbred to virtual homozygosity by Rapp (S/JR and R/JR). The S strain has been shown to have a mutation of the cytochrome P-450-dependent 11 beta,18-hydroxylase resulting in the enhanced production of 18-hydroxydeoxycorticosterone (18-OH-DOC) compared to that of the R strain. It is known that this enzyme is also responsible for the hydroxylation of deoxycorticosterone at the 19 position to produce 19-hydroxydeoxycorticosterone. Recently, the excretion of 19-nordeoxycorticosterone (19-nor-DOC), a potent mineralocorticoid, has been shown to be markedly increased in S/JR females compared to that in R/JR females consuming a high sodium diet. While the S/JR rat is spontaneously hypertensive, the course of the disease is greatly accelerated and exacerbated by a high sodium diet. If, indeed, 19-nor-DOC is responsible for the spontaneous hypertension in the S/JR rat, then its production should also be higher in the S/JR rat consuming a normal salt diet. Furthermore, since its production is suppressed by NaCl intake, the excretion should be even higher when not suppressed by a high sodium diet. We measured the urinary excretion of 19-nor-DOC, 18-OH-DOC, and corticosterone in male and female S/JR and R/JR rats consuming a normal sodium diet. The excretions of corticosterone and 18-OH-DOC were significantly higher by S/JR of both sexes than by R/JR, with the excretion by female rats being higher than that by male rats within the same strain. The hierarchy of excretion rates of 19-nor-DOC was: S/JR females greater than R/JR females greater than S/JR males greater than R/JR male rats. These studies indicate that while S/JR rats of both sexes develop higher blood pressures than the R/JR even on a standard salt intake, the excretion of 19-nor-DOC does not correlate well with their blood pressure elevation, since the normotensive female R/JR rat excretes significantly higher quantities of 19-nor-DOC than the hypertensive male S/JR rat. Thus, it is unclear whether 19-nor-DOC is playing a significant role in the pathogenesis of the hypertension in the S/JR rat. It also remains unknown whether the renal site of formation of 19-nor-DOC allows access to the mineralocorticoid target sites in the kidney.

Animals↗
PubMed1978

Effects of dietary potassium and race on urinary excretion of kallikrein and aldosterone in man.

Urinary excretion of kallikrein by 16 normal and 8 hypertensive subjects was studied at three levels of dietary potassium: 85 meq/day for 5 days, 185 meq/day for 7 days, and 25 meq/day for 10 days. Excretion of kallikrein varied directly with potassium intake and paralleled excretion of aldosterone in both normotensive and hypertensive subjects. Mean levels of excretion of kallikrein at 85, 185, and 25 meq intake of potassium were 10.8, 19.1, and 5.8 esterase U/day (EU/day), respectively, for the normotensive subjects and 8.8, 13.9, and 6.1 EU/day for the hypertensive subjects. Mean levels of excretion of kallikrein were significantly higher in white that in black subjects among normals and hypertensives [13.0 vs. 5.9 EU/day for normals (P less than 0.05) and 13.7 vs. 4.0 EU/day for hypertensives (P less than 0.05) on the 85 meq/day diet]. The parallel changes in excretion of kallikrein and aldosterone support the hypothesis that changes in effective levels of aldosterone induce changes in the excretion of kallikrein. Because of racial differences in excretion of kallikrein, matched groups should be used for comparisons of the kallikrein system in disease states.

Adult↗
PubMed1981

Urinary excretion of free and conjugated 3',5'-diiodothyronine and 3,3'-diiodothyronine.

RIAs for the estimation of 3',5'-diiodothyronine (3',5'-T2) and 3,3'-diiodothyronine (3,3'-T2) in human urine have been established. The urinary excretion of both glucuronide and sulfate conjugates of T2 and of T4, T3, and rT3 were estimated by means of enzymatic deconjugation. In healthy controls, the mean excretion (picomoles per 24 h) of free T4 was 1820, that of free T3 was 813, that of free rT3 was 77, that of free 3',5'-T2 was 13, and that of free 3,3'-T2 was 674. The total excretion of free and conjugated T4 was 2941, that of T3 was 1283, that of rT3 was 791, that of 3',5'-T2 was 709, and that of 3,3'-T2 was 2688. Significant amounts of sulfated T4 and T3 could not be demonstrated, amounts of sulfated T4 and T3 could not be demonstrated, whereas the excretion of sulfated rT3 was higher than that of glucuronidated rT3 (P less than 0.001). In contrast, glucuronidated and sulfated 3',5'-T2 as well as glucuronidated and sulfated 3,3'-T2 were found in the urine in equal amounts. In hyperthyroidism, the excretions of free and glucuronidated iodothyronines were increased, whereas the increase of the excretions of sulfated iodothyronines were less pronounced, only reaching statistical significance for 3,3'-T2 (P less than 0.02). In hypothyroidism, the excretions of both free, glucuronidated and sulfated iodothyronines were reduced. Significant amounts of sulfated T4 and T3 could not be demonstrated in urine from hyperthyroid or hypothyroid patients. Our data demonstrate that the amounts of free iodothyronines excreted in the urine vary considerably, suggesting active renal handling. The amounts of urinary glucuronidated and sulfated conjugates of the different iodothyronines studied vary considerably and are affected by thyroid function.

Cross Reactions↗
PubMed1997

Dietary alterations in plasma very low density lipoprotein levels modify renal excretion of urates in hyperuricemic-hypertriglyceridemic patients.

Hyperuricemic-hyperlipidemic patients exhibit decreased renal excretion of urates relative to purely hyperuricemic patients; also, very low density lipoprotein (VLDL) levels are inversely proportional to the amount of urate excreted. Based on this knowledge, the aim of this study was to alter VLDL levels by dietary manipulation and assess its effect on uric acid levels and renal excretion of uric acid. Thirty-six men were studied in 2 groups consisting of 20 primary hyperuricemic (group I) and 16 primary hyperuricemic-hypertriglyceridemic patients (group II). The patients were analyzed for apoproteins and lipoproteins, urate levels, and renal excretion of uric acid in a first, basal determination, after 3 weeks of a 1200-Cal diet, and after another 3 weeks of a 2500-Cal diet. After the 1200-Cal diet, patients in group I exhibited significantly decreased levels of cholesterol (P < 0.05) and apoprotein CIII (P < 0.05). There were significant differences in renal excretion of uric acid (P < 0.05) between the basal and third determinations. Patients in group II exhibited significantly decreased levels of triglycerides (P < 0.01), VLDL cholesterol (P < 0.01), VLDL triglycerides (P < 0.01), and VLDL apoprotein B (P < 0.05) after the 1200-Cal diet; all of these parameters returned to values similar to the basal levels on completion of the 2500-Cal diet. With regard to purine parameters, the low calorie diet led to significantly increased fractional excretion of uric acid (P < 0.01) and uric acid clearance (P < 0.01), both of which decreased significantly to values near basal after the 2500-Cal diet. The results obtained in this study reveal that the decreased levels of triglyceride and VLDL components that arise from a low calorie diet are accompanied by increased renal excretion of urates and that the increase in the amount of this type of lipoprotein particle with an increase in dietary energy offsets the increase in renal excretion of urate.

Adult↗
PubMed1983

Renal acid excretion in the domestic fowl.

1. In order to assess the role of uricotelism in net renal acid excretion, blood and ureteral urine samples were collected from five hens fed a commercial poultry feed (Diet A) and five hens fed a protein-rich, Na-poor feed (Diet B). All samples were analysed for pH, PCO2, ammonium, phosphate, uric acid and urates (UA + U) and inulin. 2. On Diet A, average pH in venous blood was 7.42, while urinary pH (pHu) ranged from 4.74 to 7.25. At average pHu (6.10), uric acid accounted for 52% of total acid excreted, H2PO4 for 20% and NH4 for 28%. Net acid excretion in ureteral urine was 345 muequiv h-1 kg body weight-1, or 5-10 times that observed in ureotelic vertebrates (amphibians and mammals). 3. The relative contributions of these urinary buffers to net renal acid excretion changed with pHu. Significant negative correlations exist between pHu and both total phosphate and ammonium excretion rates (P less than 0.001). Excretion rates of (UA + U) showed a positive correlation (P less than 0.05) with pHu. 4. Feeding on Diet B revealed the homeostatic power of the avian kidney. Blood pH and PCO2 were not changed relative to values in hens fed the control diet while striking increases in excretion rates of all urinary buffers (except HCO3) were observed. Average pHu fell to 5.12, and the average net renal acid excretion rate doubled.

Acid-Base Equilibrium↗
PubMed1996

Excretion and distribution of ammonia and the influence of boundary layer acidification in embryonic rainbow trout (Oncorhynchus mykiss)

This study examined ammonia excretion by embryos of the rainbow trout (Oncorhynchus mykiss). The distribution of ammonia in relation to the H+ distribution and electrical potential was determined. The influence of the pH of the unstirred layer (USL) of water next to the external surface of the embryo was also assessed. Eyed-up embryos (35&shy;40 days post-fertilization) were exposed to various external water conditions [pH 6.0, pH 10.0, 1.6 mmol l-1 NaCl, 0.0 mmol l-1 NaCl, 0.2 mmol l-1 NH4Cl, 2.5 mmol l-1 borax buffer (Na2B4O7.10H2O), 2.5 mmol l-1 Hepes, 0.1 mmol l-1 amiloride] for 30 min and ammonia excretion rates, ammonia concentration in the perivitelline fluid (PVF) and yolk, and the pH of the PVF, yolk and USL were measured. The rate of ammonia excretion was dependent, in part, on the partial pressure gradient of NH3 ( PNH3) from the PVF to the USL. Exposure to water of pH 6 increased, whereas NH4Cl or pH 10 exposure decreased, ammonia excretion rates. Elevated external Na+ levels also influenced the rate of ammonia excretion, but neither Na+-free water nor amiloride had any effect. The distribution of ammonia between the PVF and USL was dependent on the H+ distribution, but ammonia was distributed according to the electrical potential between the PVF and yolk. The USL was 0.32 pH units more acidic than the bulk water. Addition of buffer to the external water eliminated the acid USL and decreased ammonia excretion rates. We conclude that rainbow trout embryos excrete ammonia primarily as NH3, but when external Na+ levels are elevated, ammonia excretion may be independent of the PNH3 gradient. The acidic USL next to the chorion probably facilitates NH3 diffusion by maintaining the PNH3 through the conversion of NH3 to NH4+ upon entry into the USL.

Journal Article↗
PubMed1998

Salt and water relations, and nitrogen excretion, in the amphibious african freshwater crab potamonautes warreni in water and in air

Mechanisms of salt and water conservation, and nitrogen excretion, were investigated in the freshwater amphibious crab Potamonautes warreni from the High Veld of South Africa. Adaptations to fresh water were assessed as pre-adaptations to air-breathing, and nitrogen excretion was examined as a potential constraint to terrestrial excursions. P. warreni was able to regulate water and salt loss in water up to 40 % sea water, but not in 80 % sea water. The water permeability of P. warreni was low and, since 97 % of the haemolymph filtrate was reabsorbed in the antennal organ, urinary water loss was minimal (0.7 microl g-1 h-1). The minimum equilibrium [Na] of P. warreni was low (0.116 mmol l-1), as were the rates of both Na loss (0.22 micromol g-1 h-1) and Ca loss (0.29 micromol g-1 h-1). The low loss rates were due to urinary salt conservation of approximately 90 % or better and to low permeability (K'Na=0.0025; K'Ca=0.0521), and were compensated for by a high-affinity uptake mechanism (Jmax=0.76 micromol g-1 h-1 and Km=0.18 mmol l-1). Acclimating P. warreni to low Na concentrations increased maximum net Na uptake rate to 1.77 micromol g-1 h-1. Nitrogen excretion in P. warreni was almost 100 % ammoniotelic, and there was no accumulation of haemolymph or urinary ammonia or urea when in air. P. warreni was unable to excrete ammonia to air, but in water the rate of excretion was nearly 70 micromol kg-1 h-1. Crabs in amphibious conditions showed pulses of elevated NH3 excretion (350 micromol kg-1 h-1) when subsequently submerged, while for crabs breathing air for 3 days this pulse reached 4.9 mmol kg-1 h-1. Air-breathing P. warreni with artificially irrigated branchial chambers excreted double the amount of NH3 via the gills compared with crabs from amphibious conditions. Water and salt conservation form useful pre-adaptations to terrestrial forays. While the relatively low water loss extends the duration of emersion, P. warreni is required to return briefly to water to excrete stored nitrogenous waste. The nature of the store remains to be determined.

Journal Article↗
PubMed1978

Implication of renal prostaglandin E in urinary sodium excretion.

To investigate the role of renal prostaglandin in the regulation of sodium metabolism, ruinary prostaglandin E excretion, an indicator of renal prostaglandin synthesis, urinary sodium excretion, plasma renin activity and urinary aldosterone excretion were measured in 84 normal subjects and 55 patients with essential hypertension on ad lib intake of sodium. The excretion rates of urinary prostaglandin E were 736.8 +/- 32.2 ng/day in normal subjects and 394.3 +/- 28.7 ng/day in essential hypertensives. The excretion rate was significantly decreased in essential hypertensives (P less than 0.001). A significant positive correlation was found between urinary sodium excretion and urinary prostaglandin E excretion in normal subjects (r = 0.39, P less than 0.001), and in essential hypertensives (r = 0.62, P less than 0.001). There was no correlation between the renin-angiotensin-aldosterone system and urinary prostaglandin E excretion in normal subjects as well as in essential hypertensives. The present data show that renal prostaglandin might be involved in the renal handling of sodium, and prove the possibility that the decrease of renal prostaglandin synthesis is one of the etiological factors in essential hypertension.

Adolescent↗
PubMed1981

Effects of methylxanthines on urinary prostaglandin E excretion in rats.

Effect of methylxanthines (theophylline, theobromine and caffeine) on urinary prostaglandin E (PGE) excretion in male rats was studied. Oral administration of xanthines significantly increased the urinary excretion of PGE. Dose-response studies showed that the maximal excretion of urinary PGE and water was obtained by administration of theophylline (50 mg/kg), where the increase in PGE was about 20 times that of the control. The excretion of urinary sodium, potassium and chloride was also markedly increased by xanthines, particularly, theophylline. Increases in urinary PGE excretion, urine volume and electrolytes excretion were inhibited by 10 mg/kg of indomethacin administered prior to theophylline. The increase of urinary PGE excretion after theophylline administration (50 mg/kg) preceded increases in water and sodium excretion. These results suggest that renal PGE mediates, at least in part, the diuretic effect of theophylline.

Animals↗
PubMed1987

20-Dihydroisomers of cortisol and cortisone in human urine: excretion rates under different physiological conditions.

The urinary excretion rates of free cortisol and cortisone as well as of their 20-dihydroisomers have been studied in normal subjects under different physiological or pharmacological conditions. For the estimation of steroid excretion rates, a fully automated, liquid-chromatographic method was used. In normal subjects, the median steroid excretion rates of free cortisol, cortisone, 20-alpha-dihydrocortisol, 20-beta-dihydrocortisol, 20-alpha-dihydrocortisone and 20-beta-dihydrocortisone were 6.7, 8.0, 9.8, 5.2, 5.7 and 1.3 mumol/mol creatinine. The excretion rates measured at three different intervals of the day followed a circadian rhythm similar to that known for the cortisol secreting activity of the adrenal gland. After adrenal stimulation by i.v. application of 250 micrograms of tetracosactide hexaacetate, (Synacthen, corticotropin beta 1-24) excretion of urinary cortisol was significantly higher than those of the other steroids. During a 24 h infusion of corticotropin beta 1-24, the excretion rates of cortisol and its C-20 reduced isomers increased to a significantly greater extent than those of cortisone and its C-20 reduced isomers. During a four-hour infusion of hydrocortisone, the relative increase of cortisol excretion was greater than that of the other steroids. During a five-hour infusion of metyrapone at different dosages, the excretion of all steroids decreased in a dose-dependent manner. The present data indicate that the 20-dihydroisomers of cortisol and cortisone in human urine primarily originate from the peripheral metabolism of cortisol rather than from adrenal secretion.(ABSTRACT TRUNCATED AT 250 WORDS)

Circadian Rhythm↗
PubMed1983

[Biliary excretion of diethyl lead after administration of tetraethyl lead in rabbits].

In order to investigate into whether the large amount of inorganic lead excreted into the feces following intravenous injection of tetraethyl lead to rabbits is derived from the diethyl lead excreted into the bile, we administered 12 mg/kg of tetraethyl lead to rabbits which had been fistulated into the bile duct for taking the bile out of the body. The total lead excreted into the bile during the first 24 hours after the injection of tetraethyl lead amounted to about 8% of the injected amount of lead (with 97% of the excreted lead made up of diethyl lead). The amount of total lead contained in the cecal contents of unfistulated rabbits 24 hours after the injection of tetraethyl lead was equivalent to about 12% of the injected amount of lead (with inorganic lead accounting for about 90% of the excreted lead), but the counterpart of the fistulated rabbits was equivalent only to about 0.6%. The amount of lead excreted into the bile, when measured in terms of the total lead content of the liver, was slightly less in the fistulated rabbits than in the unfistulated ones. These findings indicated that the amount of total lead excreted into the bile of the fistulated rabbits was almost the same as that contained in the cecal contents of unfistulated rabbits, and that the major portion of the lead contained in the cecal contents or feces was composed of inorganic lead. From these results, we came to the conclusion that the large amount of inorganic lead detected in the feces after the injection of tetraethyl lead is derived from the diethyl lead excreted into the bile.

Animals↗
PubMed1993

Urinary epidermal growth factor is excreted from the rat isolated perfused kidney in the absence of plasma.

Large amounts of epidermal growth factor (EGF) are excreted in urine and the majority of this urinary EGF appears to be of renal origin. EGF is synthesized in the kidneys as a membrane-bound 160 kDa precursor, in the thick ascending limb of Henle and in the early part of the distal convoluted tubule. Very little is known about how EGF is released from cell membranes into urine but proteolytic cleavage of the membrane-bound EGF precursor seems likely. The purpose of this study was to examine whether plasma constituents are necessary for urinary excretion of EGF. In the rat isolated kidney perfused at a pressure of 90 mmHg with a modified Krebs-Henseleit buffer containing oncotic agents, the quantity of EGF excreted into the ureteral effluent was 67% of the amount excreted by the rat kidney in vivo. The EGF excreted by the isolated kidney behaved like urinary EGF upon gel filtration. Administration of the proteinase inhibitor aprotinin reduced urinary EGF excretion from the rat isolated perfused kidney by approximately 50%. In conclusion, the rat isolated perfused kidney excreted significant amounts of urinary EGF without having access to plasma, and EGF excretion was reduced by aprotinin. This is further evidence suggesting an intrarenal source of urinary EGF and suggests that the EGF precursor in the rat kidney is processed by enzyme(s) of renal origin.

Animals↗
PubMed1990

Evidence that urodilatin, rather than ANP, regulates renal sodium excretion.

Urodilatin, a closely related member of the atrial peptide family, was discovered recently in human urine. Urodilatin (ANP 95-126) is believed to be produced within the kidney and is natriuretic; evidence indicates that most of the ANP-like immunoreactivity in the kidney elutes with urodilatin rather than with ANP. Moreover, urodilatin is little affected by renal enzymes that inactivate atriopeptin. To determine the relative importance of urodilatin versus ANP in the regulation of renal sodium excretion, we studied intact and cardiac-denervated conscious dogs under three experimental conditions: (1) spontaneous sodium excretion, (2) intravenous infusion of saline, and (3) left atrial distension. Urodilatin was measured in urine with a newly developed radioimmunoassay that selectively measures urodilatin without any cross-reactivity with alpha-human atrial natriuretic peptide (alpha-hANP); alpha-hANP was measured in plasma by radio-immunoassay because it is rapidly inactivated in the kidney by enzymatic activity. In each group of experiments, sodium excretion correlated better with urodilatin than it did with circulating alpha-hANP. The correlation coefficient (r value) between urodilatin excretion and renal sodium excretion exceeded 0.8 in 13 of 18 experiments and was below 0.6 in only 2 experiments. On the other hand, the correlation between circulating atriopeptin and sodium excretion exceeded 0.8 in only 3 of 18 experiments and was below 0.6 in 10 experiments. A negative correlation between plasma atriopeptin and renal sodium excretion was observed during left atrial distension in the cardiac-denervated dogs. These results and other considerations suggest that urodilatin, rather than atriopeptin, is the member of the ANP family that is primarily involved in the regulation of renal sodium excretion.

Animals↗
PubMed2001

Development of renal potassium excretion capacity in the neonatal rat.

We investigated the capacity of newborn rats to excrete an acute potassium load to understand the development of a renal potassium excretion system. Three groups of the rats (7-14 d) were used to collect urine periodically over 6 h after oral infusion of potassium: control (no potassium loading) and low- and high-potassium-loaded rats. In the low-potassium-loaded group, infused with about 0.6 microEq of potassium chloride/g body wt., the rate of renal potassium excretion increased from 0.08 plus minus 0.02 (7 d) to 0.13 plus minus 0.02 (10 d) and 0.21 plus minus 0.03 (14 d) microEq/h/g body wt. The high-potassium-loaded rats (1.5-2.8 microEq/g body wt. potassium load) excreted potassium at a higher rate of 0.18 +/- 0.05 (7 d), 0.30 +/- 0.02 (10 d), and 0.45 +/- 0.10 (14 d) microEq/h/g body wt. They excreted 77% (7 d), 76% (10 d), and 95% (14 d) of the potassium load. These values were much larger than the rate of 0.026 microEq/h/g body wt. of the control rats and of 0.08 microEq/h/g body wt., a mean potassium excretion rate during development from 7 to 14 d calculated from the data in the previous study (Kanno T et al.: J. Pediatr. Gastr. Nutr. 24: 242-252, 1997). In the same period, serum potassium concentration in the newborn rats decreased significantly (p < 0.01) from 7.2 +/- 0.1 (7 d) to 6.7 +/- 0.1 mEq/l (14 d). All these results suggest that a renal potassium excretion system in the rat develops at least in the second week of life, and its capacity is high enough to excrete the daily potassium intake.

Animals↗
PubMed1990

Excretion of tetramethyllead, trimethyllead, dimethyllead and inorganic lead after injection of tetramethyllead to rabbits.

Rabbits were divided to groups of 3, and injected either 9.9 mg of tetramethyllead (Me4Pb)/kg of body weight (7.7 mg Pb/kg) or 39.7 mg/kg (30.8 mg Pb/kg) into the ear vein once only, respectively, and urinary and fecal excretions of lead were studied for chemical species and total lead during the following 7 days. In the group injected 9.9 mg/kg, the urinary total lead excretion was composed of about 73% dimethyllead (Me2Pb2+), about 19% trimethyllead (Me3Pb+), about 6% inorganic lead (Pb2+), and about 2% Me4Pb on the day following the injection, and 100% Me3Pb+ 7 days after the injection. In the group injected 39.7 mg/kg, the urinary total lead excretion was composed of about 67% Me2Pb2+, about 14% Me3Pb+, about 17% Pb2+, and about 2% Me4Pb on the day following the injection, and about 8% Me2Pb2+, about 74% Me3Pb+, about 17% Pb2+, and about 1% Me4Pb 7 days after the injection. In both groups, the fecal total lead excretion during 7 days after the injection was entirely composed of Pb2+. During the 7 days, 1-3% of either administered dose was excreted in the urine, and 7-19% in the feces. The urinary total lead excretion in the rabbits injected Me4Pb was similar to that in the rabbits injected tetraethyllead, but the fecal total lead excretion in the former was extremely smaller. This extremely small fecal excretion of total lead appeared to have resulted from the less elimination of lead into the bile of Me4Pb-injected rabbits.

Animals↗