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PubMed2005

Biliary excretion of olmesartan, an anigotensin II receptor antagonist, in the rat.

BACKGROUND AND AIM: Olmesartan (RNH-6270) is a newly developed anigotensin II receptor antagonist, and has been reported to be excreted into feces. To examine the mechanism of the biliary excretion of olmesartan, we studied its biliary excretion in rats. METHODS: The biliary excretion of olmesartan in Eisai hyperbilirubinemic rats (EHBR), a multidrug resistance protein 2-deficient rat, was compared with control rats, and the effect of organic anions and cation and bile acids on the biliary excretion of olmesartan was studied in control rats. RESULTS: The biliary excretion of olmesartan was markedly delayed in EHBR. The biliary excretion of olmesartan was inhibited by sulfobromophthalein, cefpiramide and pravastatin, but was not inhibited by taurocholate or tauroursodeoxycholate. Vinblastine inhibited and phenothiazine treatment increased the biliary excretion of olmesartan. CONCLUSIONS: These findings suggest that olmesartan is excreted into the bile mainly by multidrug resistance protein 2 and partly by P-glycoprotein.

ATP-Binding Cassette Transporters↗
PubMed1993

Increased urinary excretion of human cytomegalovirus in children with malignancy: detection by polymerase chain reaction.

Human cytomegalovirus (HCMV) is one of the most important agents causing opportunistic infections in immunocompromised hosts. In this study, we examined the urinary excretion of HCMV in children with malignancy using polymerase chain reaction (PCR). Urine samples were collected from on-therapy, off-therapy patients with malignancy, and healthy controls. A simple DNA extraction method using glass powder was employed, and inhibitory effect of urine on PCR was prevented. For PCR, a pair of primers from the HCMV major immediate early gene sequence was used. Among patients who received intensive chemotherapy, 52.0% had urinary HCMV excretion after the chemotherapy course. In contrast, off-therapy patients and healthy controls showed a lower incidence of urinary HCMV excretion (20.4 and 8.7%, respectively). The incidence of HCMV urinary excretion in the on-therapy group was significantly higher than healthy controls (P < 0.05). In the on-therapy group, the total white blood cell count of the virus excreters was lower than that of non-excreters. The incidence of HCMV excretion was high in on-therapy patients. Most of the virus excreters were seropositive, so their viruria was thought to be caused by reactivation. Repeated monitoring of virus excretion by this rapid and simple method may be useful to detect HCMV infection early and to control it in such patients.

Adolescent↗
PubMed1991

The interaction between atrial natriuretic peptides and angiotensin II in controlling sodium and water excretion in the rat.

1. The present study was designed to determine how the natriuretic and diuretic actions of atrial natriuretic peptides were modulated by circulating angiotensin II. 2. In sodium pentobarbitone-anaesthetized rats, administration of bolus doses of atriopeptin III (1000 ng kg-1) had no effect on blood pressure, renal blood flow, or glomerular filtration rate but caused reversible increases (all P less than 0.001) in urine flow, of 53.9 +/- 14.4 microliters kg-1 min-1, absolute sodium excretion, of 13.4 +/- 2.9 mumol kg-1 min-1 and fractional sodium excretion of 3.26 +/- 0.74%. Similar effects were seen following a second dose of the atriopeptin III. 3. Following blockade of the renin-angiotensin system with captopril (900 micrograms kg-1 h-1), control levels of blood pressure and haemodynamics were unchanged but there were significant (all P less than 0.001) increases in urine flow, from 39.96 +/- 5.05 to 88.70 +/- 8.41 microliters kg-1 min-1, absolute sodium excretion, from 8.35 +/- 1.08 to 21.62 +/- 1.62 mumol kg-1 min-1 and fractional sodium excretion, from 3.82 +/- 0.23 to 5.34 +/- 0.32%. Under these conditions, atriopeptin III-induced increases in urine flow (110.2 +/- 8.7 versus 43.9 +/- 6.2 microliters kg-1 min-1) absolute (24.0 +/- 1.8 versus 9.3 +/- 1.2 mumol kg-1 min-1) and fractional (5.16 +/- 0.24 versus 2.08 +/- 0.33%) sodium excretions were significantly (P less than 0.001) greater.4. In another group of rats given captopril, angiotensin II at ongkg-1 min1 was also infused; this had no effect on blood pressure or renal haemodynamics, but partially restored basal levels of sodium and water excretion to those obtained before captopril. Atriopeptin III reversibly increased urine flow and absolute sodium excretion to the same degree as that obtained without captopril, but fractional sodium excretion was significantly larger than that obtained in the absence of captopril. In rats infused with angiotensin II at 15ngkg-1min1' together with the captopril the basal levels of fluid output were unchanged, while the magnitudes of the urine flow and sodium excretory responses to atriopeptin III were identical to those obtained before captopril and angiotensin II.5. In animals subjected to two weeks of a low-sodium diet, atriopeptin III reversibly increased urine flow, absolute and fractional sodium excretions by between 53% and 74%; these responses were significantly (P < 0.001) smaller than those obtained in sodium replete rats. Administration of atriopeptin III, to low sodium diet rats given captopril, induced excretory responses which were significantly larger than those obtained in the absence of captopril. 6. The findings of this investigation demonstrate that in acute situations, angiotensin II exerts an important modulatory influence on the natriuretic potency of the atrial peptides by attenuating their action on the kidney. Long-term activation of the renin-angiotensin system depresses the renal excretory responses to atrial natriuretic peptides but suppression of angiotensin II production only partially restores the responsiveness of the kidney.

Angiotensin II↗
PubMed1991

Nifedipine increases urinary excretion of prostacyclin metabolite in hypertensive pregnancy.

Renal prostanoid excretion was investigated in nine hypertensive pregnant patients before and during treatment with nifedipine 10 mg orally t.i.d. Urinary excretion of prostacyclin (measured as 6-ketoprostaglandin F1 alpha, 6-keto-PGF1 alpha) increased by 77% during nifedipine treatment (P less than 0.05). No changes were found in prostaglandin E2 (PGE2) and thromboxane A2 (as thromboxane B2, TXB2) excretions. A significant reduction in blood pressure did not correlate with an increase in 6-keto-PGF1 alpha excretion. Plasma prekallikrein and urinary kallikrein and catecholamine excretions remained unaltered. In six normotensive non-pregnant women, increase in 6-keto-PGF1 alpha excretion during nifedipine treatment was not significant. No changes in PGE2 and TXB2 excretions were found, whereas plasma prekallikrein was reduced (P less than 0.05) and urinary excretion of kallikrein (P less than 0.05) and noradrenaline (P = 0.06) increased under nifedipine. The results suggest that nifedipine enhances the renal 6-keto-PGF1 alpha excretion in hypertensive pregnancy.

6-Ketoprostaglandin F1 alpha↗
PubMed1982

Commentary on the reduced urinary noradrenaline excretion following cold stress and exercise in physically trained rats.

Urinary catecholamine excretions of rats trained by swimming or running were compared with those of cold-acclimated rats and controls i.e. sedentary warm-acclimated rats. During cold stress the trained rats excreted less noradrenaline (NA) than did controls. In fact rats trained by swimming excreted less NA than did cold-acclimated rats, while rats trained by running excreted about the same amount as did cold-acclimated rats. 2 h of swimming increased the urinary catecholamine (CA) excretion of all groups but trained rats excreted less NA than did controls and cold-acclimated rats, which had excretions of similar magnitude. The NA excretions of the two trained groups never deviated statistically from each other. It is concluded that concerning NA requirement in order to maintain homeostasis, training produces "cross tolerance" to cold stress but cold-acclimation does not produce "cross tolerance" to acute exercise. Furthermore the positive effect of training on NA excretion during the stress of cold or that of acute exercise seems essentially to be an effect of increased locomotor activity as such regardless of the type of training. It is also suggested that increased levels of locomotor activity of the rat may be of importance for seasonal acclimation of the species by increasing its tolerance to cold.

Animals↗
PubMed1988

Atrial natriuretic factor, urinary catechol compounds and electrolyte excretion in rats during normal hydration and isotonic volume expansion. Influence of dopamine receptor blockade.

To investigate the influence of acute isotonic volume expansion (VE) on the plasma concentration of atrial natriuretic factor (ANF), the excretion of catechol compounds and electrolytes and the whole kidney glomerular filtration rate (GFR), these variables were measured before and during 60 min of VE (2% of body weight per hour). Atrial natriuretic factor was measured at the end of the experiment. In a control group (n = 7) without volume expansion, plasma ANF was 58 +/- 4 pg ml-1. The excretion of sodium, dopamine (DA), 3,4-dihydroxyphenylacetic acid (DOPAC), noradrenaline (NA) and GFR did not change during the control study. In VE animals (n = 7) plasma ANF was 82 +/- 7 pg ml-1, significantly higher than in the control group. Sodium excretion increased more than 17-fold. The excretion of the DA increased by 38% and that of DOPAC by 30%. Noradrenaline excretion remained unchanged while GFR increased by 20%. In haloperidol-pretreated animals subjected to VE (n = 7), plasma ANF was 81 +/- 8 pg ml-1 during VE, significantly higher than in the control animals. Although the sodium excretion increased more than ninefold in this group during VE, this increase was only 55% of that in the VE group not given haloperidol. The DA and DOPAC excretion was increased by haloperidol, indicating a feedback effect of receptor blockade. DOPAC excretion was not increased further by VE, but the excretion of DA increased by 15% and GFR increased by 19%.(ABSTRACT TRUNCATED AT 250 WORDS)

3,4-Dihydroxyphenylacetic Acid↗
PubMed1976

The effect of plasma potassium in determining normal rates of excretion of potassium in dogs.

Doses of 5-15 mmol KCl or KHCO3 (less than the daily intake in food) given by stomach tube or intravenous infusion, produced increases in plasma K and in K excretion, the time delay between change in plasma K and rate of excretion being minimal. Without doses of K salts in control experiments, plasma K concentration was about 4 mmol/1 and K excretion about 5 mumol/min. After doses of KCl or KHCO3, plasma K and rate of excretion of K both increased, increase of 0-5 mmol/1 in plasma K being associated with an increase of about 35 mumo1/min in K excretion. Increased excretion of K was accompanied by a small increase in Na excretion. Excretion of both C1 and HCO3 increased, C1 more after HCO3 more after KHCO3. The results indicate that within normal ranges, plasma K is an important factor determining the rate of excretion of K.

Animals↗
PubMed1974

Relationship between glucose and sodium excretion in the new-born dog.

1. The relationship between renal glucose and sodium excretion was studied in thirty-three new-born dogs aged 1-14 days and in ten adult dogs.2. Glucose was infused into the animals at rates sufficient to produce an amount of filtered glucose at least 1.5 times the tubular transport of glucose (saturating glucose load). In both puppies and adults tubular glucose reabsorption at saturating glucose loads varied directly with the glomerular filtration rate (r = 0.54 and 0.73 respectively, P < 0.01 for both).3. In the puppy, as the fraction of filtered sodium excreted (C(Na)/C(In)) increased from 0.05 to 0.45, the ratio, renal tubular glucose transport divided by glomerular filtration rate at saturating glucose loads, (T(G)/GFR)(m), decreased from 3.7 to 1.7 mg/ml. (r = -0.75, P < 0.01). In the adult C(Na)/C(In) was below 0.08 in all experiments and (T(G)/GFR)(m) was within the 95% confidence limits predicted by regression analysis of the data from puppies. Although mean (T(G)/GFR)(m) was greater in the adult than in the puppy (P < 0.01), when puppies had C(Na)/C(In) similar to that for adults, they had (T(G)/GFR)(m) values equivalent to that for the adult.4. There was excellent correlation between glucose excretion and water excretion for both adult and new-born dogs (r = 0.93 and 0.87, respectively). However, for any glucose loss, water loss was greater in the puppy than in the adult (P < 0.01).5. During the control period total sodium excretion (per gram kidney) and C(Na)/C(In) were similar in the new-born and adult dog. However, during glucose loading, the puppies excreted more sodium and had a higher C(Na)/C(In) than did the adult, although glucose excretion was greater in the adult than in the puppy (P < 0.01 for all comparisons).6. Glomerular blood flow, as measured by radioactive microspheres, was redistributed towards inner cortical nephrons during glucose loading in the puppy. There was no such redistribution of glomerular blood flow in the adult.7. Sodium reabsorption beyond the proximal tubule was blocked with ethacrynic acid and chlorothiazide. In the puppy, the increase of C(Na)/C(In) following a glucose load was the same whether the glucose load followed control or distal blockade collections, suggesting that reductions of sodium reabsorption following a glucose load probably came from the proximal tubule. C(Na)/C(In) during glucose loading plus distal blockade was significantly (P < 0.01) higher in the puppy (0.598) than in the adult (0.280), indicating that glucose diuresis produced a greater inhibition of proximal tubular sodium reabsorption in the new-born than in the adult dog. These results support the hypothesis that the high sodium excretion rate during glucose diuresis in the new-born dogs appears to be due to the greater sensitivity of the neonatal proximal tubule to the osmotic effect of glucose. When presented with a glucose osmotic load the new-born dog diminishes net proximal sodium reabsorption more than does the adult and thus depresses tubular glucose reabsorption to a greater extent. The lower values of maximal glucose transport rates found in new-born animals may be related, therefore, to the higher fractional sodium excretion rates during glucose diuresis rather than to a diminished intrinsic glucose transport capacity in the new-born kidney.

Age Factors↗
PubMed2003

Induction of multidrug resistance protein 3 in rat liver is associated with altered vectorial excretion of acetaminophen metabolites.

Treatment with the microsomal enzyme inducer trans-stilbene oxide (TSO) can decrease biliary excretion of acetaminophen-glucuronide (AA-GLUC) and increase efflux of AA-GLUC into blood. The hepatic canalicular multidrug resistance protein (Mrp) 2 and sinusoidal protein Mrp3 transport AA-GLUC conjugates into bile and blood, respectively. Thus, TSO-induced alterations in the vectorial excretion of AA-GLUC may occur via increased hepatic Mrp3 levels. The goal of this study was to determine whether TSO, diallyl sulfide (DAS), and oltipraz (OLT) treatments can up-regulate Mrp3 protein expression, and whether treatment with DAS and OLT can correspondingly increase hepatovascular efflux of AA metabolites. Rats were administered phenobarbital, TSO, DAS, OLT, or vehicle for 4 days. Interestingly, all of the chemicals increased the plasma concentration and urinary excretion of AA-GLUC and decreased its biliary excretion. In control animals, approximately 77% and 23% of AA-GLUC was excreted into bile or urine, respectively, whereas with inducer-pretreated animals, <32% of AA-GLUC was excreted into bile and >68% was excreted into urine. Correspondingly, all of the compounds increased hepatic Mrp3 mRNA levels by 13- to 37-fold and protein levels by 2- to 6-fold, respectively. In conclusion, these studies correlate increased Mrp3 protein levels in liver with increased hepatovascular excretion of AA-GLUC and suggest that induction of Mrp3 affects the route of drug excretion.

ATP Binding Cassette Transporter, Subfamily B↗
PubMed2003

Increased urinary excretion of aquaporin 2 in patients with liver cirrhosis.

BACKGROUND AND AIM: Water retention is a major clinical problem in patients with liver cirrhosis. Recent research suggests that renal aquaporins may be pathophysiologically involved in this condition. The aim of the present cross sectional study of patients with liver cirrhosis was to determine if 24 hour urinary excretion of renal aquaporin 2 (AQP2) differed from that of healthy control subjects and if such excretion was related to the severity of liver disease and to the patient's water balance. RESULTS: Twenty four hour urinary excretion of AQP2 and free water clearance were measured in 33 stable cirrhosis patients on usual medication and in eight healthy subjects. AQP2 excretion, quantitated by immunoblotting, was eight times higher in cirrhosis patients than in controls (0.167 (0.270) U/day v 0.021 (0.017); p<0.05). Stratification according to clinical manifestations (Child- Pugh classes) revealed that it increased with the clinical severity of cirrhosis (class A 0.04 (0.04); class B 0.09 (0.16); class C 0.31 (0.35); p<0.05) but was not related to liver function, as measured by galactose elimination capacity. Excretion correlated inversely with free water clearance (rho=-0.57, p<0.01). It was higher in patients with oesophagogastric varices but not in those with ascites. Plasma vasopressin concentrations were not related to AQP2 excretion and there was no relation to dose or type of diuretic treatment. CONCLUSIONS: Urinary AQP2 excretion was increased in patients with cirrhosis. Moreover, urinary AQP2 excretion increased with severity of cirrhosis in parallel with impairment of free water clearance. This suggests a functional association between increased AQP2 excretion and increased renal reabsorption of water in cirrhosis.

Adult↗
PubMed1987

Epidemiology of Salmonella typhimurium infection in calves: excretion of S typhimurium in the faeces of calves in different management systems.

Twenty-five batches of market-purchased calves, comprising 589 animals on 11 farms, were examined for the excretion of salmonellas for at least 28 days after their arrival. Salmonellas were found in 217 (51 per cent) of 423 calves from 18 of 21 batches on nine farms. The calves were housed in single pens on eight farms and in groups on the others. The trends in new excreters and the proportion of Salmonella typhimurium excreters were similar in both types of housing, a peak of excretion which was slightly higher in single penned calves, being reached 18 to 19 days after arrival. New excreters were found at most samplings in both types of housing, but the peak of new excreters appeared earlier and declined sooner in single penned calves. On average, single penned animals excreted salmonellas longer. Salmonella dublin was found only in single-penned calves, and the trend in excretion was similar to that for S typhimurium in single-penned calves except that the peak was at about 28 days. Prophylactic feeding of antibiotics was practised on nine farms, but appeared to have no influence on the excretion of salmonellas. Salmonellas were isolated from the environment in six of nine farms studied, even after cleaning and disinfection. It is suggested that the persistence of salmonellas in the environment deserves more attention in the formulation of control programmes.

Animals↗
PubMed1994

Biliary excretion of plasma non-transferrin-bound iron in rats: pathogenetic importance in iron-overload disorders.

Plasma non-transferrin-bound iron (NTB-iron) is a potentially toxic form of iron, which is efficiently taken up by the normal, as well as the chronically iron-overloaded liver. In fact, NTB-iron may represent the major source of iron gaining access to hepatocytes in the iron-loaded state. We postulated that efficient biliary excretion of this form of iron could protect against iron-related hepatocellular injury. To characterize the biliary excretion of NTB-iron in intact normal and iron-loaded rats, the plasma disappearance and biliary excretion kinetics of plasma 55Fe-labeled NTB-iron were determined. In normal rats, prompt biliary excretion of plasma NTB-iron was evident, with peak radioactivity approximately 10 min after 55Fe injection (4.1% mean recovery at 3 h). In contrast, biliary iron excretion in iron-loaded rats was minimal (0.1%). In normal rats, a marked increase in biliary excretion of plasma NTB-iron was observed after intravenous desferrioxamine (mean recovery 20.9%) and the new oral iron chelator 1,2-dimethyl-3-hydroxypyrid-4-one administered intravenously (mean recovery 16.1%) or orally (11.4%). In iron-loaded rats, the cumulative recoveries of 55Fe in bile achieved by chelators were lower than in controls (7.6, 3.9, and 3.7%, respectively). Collectively, these findings demonstrate that 1) the normal liver rapidly excretes significant amounts of plasma NTB-iron in bile; 2) the iron-loaded liver exhibits a marked decrease in the capacity to excrete plasma NTB-iron into bile; and 3) chelating agents greatly enhance the biliary excretion of plasma NTB-iron, although the response in terms of cumulative recoveries is less pronounced in the iron-loaded state.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1989

Amiloride effect on diurnal cyclic Na and K excretion in rats.

Amiloride was administered to rats during the peak and minimum of Na and K diurnal rhythmic excretion (i.e., during early dark phase and early light phase). In rats receiving a normal-K diet (2.34 meq/day) amiloride decreased K excretion from 186 to 37 mueq/h (dark phase) and from 31 to 4 mueq/h (light phase). Amiloride increased Na excretion from 91 to 344 mueq/h (dark phase) and from 35 to 164 mueq/h (light phase). Rats receiving a high-K diet (10.4 meq/day) showed a higher diurnal peak and minimum for K excretion. During high-K intake, amiloride decreased K excretion from 787 to 191 mueq/h (dark phase) and from 197 to 40 mueq/h (light phase) and increased Na excretion from 237 to 891 mueq/h (dark phase) and from 31 to 222 mueq/h (light phase). Whenever given, amiloride reduced K excretion to approximately 20% of control excretion. It is concluded that rhythmic changes in amiloride-sensitive distal transport are largely, but not entirely, responsible for the diurnal K cycle, but do not cause the concurrent Na cycle. Thus the diurnal cycles in Na and K are expressed through changes in different transport mechanisms. In rats maintained on a high-K diet there is an increase in rhythmic K secretion and Na reabsorption by amiloride-sensitive transport. To maintain Na excretion unchanged, Na reabsorption must be correspondingly depressed at an amiloride-insensitive site.

Amiloride↗
PubMed1985

Abnormalities in kallikrein excretion in spontaneously hypertensive rats.

Experiments were conducted to examine kallikrein excretion in 12-wk-old anesthetized and conscious Okamoto-Aoki spontaneously hypertensive rats (SHR) and normotensive Wistar-Kyoto rats (WKY). Urinary excretion of active and total kallikrein was determined at spontaneous pressures and in response to acute decreases in renal perfusion pressure (RPP; suprarenal aortic constriction). Under basal conditions, active kallikrein excretion was lower in SHR compared with WKY whether conscious (4.4 +/- 1.7 vs. 9.4 +/- 1.3 pkat . min-1 . g kidney wt-1) or anesthetized (5.7 +/- 1.3 vs. 10.4 +/- 1.7). In both anesthetized SHR and WKY, excretion of active and total kallikrein was directly related to RPP after 20 mmHg decrements in RPP and was depressed in SHR at each pressure level. The slope of the relation between active kallikrein excretion and pressure was less in SHR (0.06 +/- 0.01 vs. 0.14 +/- 0.05 pkat . min-1 . g kidney wt-1 . mmHg-1). Thus kallikrein excretion is set at a lower level in SHR and is less responsive to changes in RPP. These strain differences are not related to urine flow, Na excretion, or glomerular filtration rate (GFR) since the values were the same in both strains at each pressure level. Analysis of covariance indicated a significant correlation between active kallikrein excretion and RPP in WKY and SHR, with RPP accounting for 92% of the variation in the kallikrein data. GFR, Na excretion, and urine flow rate were not significantly correlated to active kallikrein and were responsible for only 2% of the variation.(ABSTRACT TRUNCATED AT 250 WORDS)

Anesthesia, General↗
PubMed1985

Role of citrate excretion in acid-base balance in diuretic-induced alkalosis in the rat.

Studies were performed to assess the role of changes in the excretion of citrate, a metabolic precursor of bicarbonate, in acid-base balance in diuretic-induced metabolic alkalosis. Rats on a low-chloride diet with sodium sulfate added were studied during a base-line period, 3 days of furosemide administration, and 4 days post-furosemide. During the period of furosemide administration, net acid excretion and plasma bicarbonate concentration increased. In the post-furosemide period, net acid excretion remained higher than base line but plasma bicarbonate concentration did not increase further. Citrate excretion was significantly higher in the post-furosemide period than in base line. Studies substituting sodium neutral phosphate or sodium bicarbonate for dietary sodium sulfate demonstrated greater increases in net acid excretion post-furosemide and, again, no increase in plasma bicarbonate concentration during this period. Citrate excretion was greater than in the sulfate group. The increment in citrate excretion was proportional to the base "load," defined with respect to changes in net acid excretion and/or dietary bicarbonate. Thus, in these studies alterations of base excretion in the form of citrate play an important role in acid-base balance during diuretic-induced metabolic alkalosis.

Acid-Base Equilibrium↗
PubMed1988

Complementary role of citrate and bicarbonate excretion in acid-base balance in the rat.

Studies were performed to evaluate whether alterations in the excretion of citrate, a metabolic precursor of bicarbonate, play a quantitatively important role in acid-base balance during bicarbonate feeding in the rat. Potassium depletion (K-DEPL), chloride depletion (Cl-DEPL), or potassium plus chloride depletion (KCl-DEPL) was produced by eliminating potassium, chloride, or potassium chloride from the diet. After 3 days of depletion, sodium bicarbonate (4,000 mueq/24 h) was added to the diet for 7 days. In all groups plasma bicarbonate concentration increased minimally during bicarbonate administration and was similar to normal controls receiving bicarbonate. In K-DEPL, citrate excretion was less than normal but bicarbonate excretion was greater than normal. In Cl-DEPL, bicarbonate excretion was less than normal but citrate excretion was greater than normal. In KCl-DEPL, bicarbonate and citrate excretion were similar to normal. Sodium bicarbonate was also administered to K-DEPL and KCl-DEPL rats in which plasma bicarbonate concentration averaged 32.9 meq/1. The reciprocal relationship between citrate and bicarbonate excretion was not altered by the profound metabolic alkalosis. Again, plasma bicarbonate concentration changed little with sodium bicarbonate administration. These studies suggest that the ability to excrete a base load remains intact despite potassium or chloride depletion or metabolic alkalosis. Complementary alterations of citrate and bicarbonate excretion play an important role in acid-base balance under these conditions.

Acid-Base Equilibrium↗
PubMed1988

Endogenous ANP augments fractional excretion of Pi, Ca, and Na in rats with reduced renal mass.

Atrial natriuretic peptide (ANP) infusion increases fractional excretion of many solutes including sodium, chloride, bicarbonate, phosphate, calcium, and magnesium. Because fractional excretion of these solutes increases with advancing renal disease, and because plasma ANP levels are known to be elevated in chronic renal failure, we sought to determine whether ANP mediates increased solute excretion rates per nephron in rats following extensive renal ablation, a model of chronic renal failure. Because sodium restriction decreases plasma ANP levels in the setting of reduced renal mass, we also determined the effect of sodium restriction on sodium, phosphate, calcium, and magnesium excretion rates in rats with 5/6 nephrectomy (NX). We also assessed whether high endogenous ANP levels influence fractional sodium, phosphate, calcium, and magnesium excretion in rats with 5/6 NX, by inhibiting ANP action via infusion of a high-affinity ANP antiserum. Whole-kidney glomerular filtration rate in 5/6 NX rats averaged approximately one-third that of shams, and plasma ANP levels were significantly elevated in these rats above those of shams, but to a lesser extent in rats on low- vs. high-salt intakes. Fractional sodium, phosphate, and calcium, but not magnesium excretion rates were significantly greater in 5/6 NX rats on the higher sodium intake compared with those in 5/6 NX rats on the lower sodium intake. Moreover, in 5/6 NX rats on the higher sodium intake, ANP antiserum significantly reduced fractional sodium, phosphate, and calcium excretion, but was without effect on magnesium excretion. These data implicate endogenous ANP in promoting the adaptive increase in sodium, phosphate, calcium, but not magnesium excretion per nephron in chronic renal disease.

Animals↗
PubMed1994

Relationship between fat-free mass and urinary excretion of creatinine and 3-methylhistidine in adult humans.

The urinary excretion of endogenous creatinine (CRTN) and 3-methylhistidine (3-MH) has been proposed as a predictor of fat-free mass (FFM) in healthy subjects. In this study, we report the relationship between FFM, estimated by densitometry plus deuterium dilution, and daily urinary excretion of CRTN and 3-MH in a sample of 20 healthy adult subjects of both sexes. 3-MH and CRTN were measured in 2 days of urine collection, which followed 4 days of meat-free diet. Meat-free diet was maintained throughout the period of urine collection. The mean of 2 days of excretion of 3-MH was 237.7 +/- 87.3 (SD) and 138.9 +/- 31.2 mumol/day in men and women, respectively. The mean CRTN excretion was 1.51 +/- 0.22 and 0.98 +/- 0.15 g/day in men and women, respectively. CRTN excretion was found well associated with FFM (R2 = 0.89; P < 0.0001), whereas 3-MH was lightly associated with FFM (R2 = 0.33; P < 0.01). Residuals from the regression of 3-MH vs. FFM were found to be correlated with CRTN excretion and FFM (R2 = 0.57 and 0.67, respectively), suggesting that muscularity and the absolute amount of lean mass are relevant for the error in predicting FFM from 3-MH excretion. Data confirm that urinary CRTN excretion can be an expedient indirect method for evaluating body composition in healthy adult subjects. Data also suggest that the relationship between 3-MH and FFM is complex, limiting the possibility of predicting body composition from the excretion of this metabolite.

Adult↗