Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “AMINOHIPPURIC ACID”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 685 records · Page 38Linked to original sources
PubMed1979

Renal effects of propranolol, practolol and butoxamine in pentobarbital-anesthetized rats.

The renal effects of the beta-adrenergic blockers, propranolol, practolol and butoxamine, were examined in pentobarbital-anesthetized rats. All the beta-blockers, infused i.v., increased urine volume (V), urinary sodium excretion (UNaV) and p-aminohippuric acid clearance without change in inulin clearance. Indomethacin, an inhibitor of prostaglandin biosynthesis, did not affect the renal effects of these beta-blockers. Phentolamine abolished the renal effects of practolol, but not those of propranolol and butoxamine. Haloperidol abolished the renal effects of propranolol and butoxamine, but not those of practolol. A high correlation was found between the increased UNaV and the increased urinary phosphate excretion by butoxamine but not by propranolol and practolol. Therefore, it is suggested that alpha-adrenergic stimulation is involved in the mechanism of diuresis by practolol, a beta1-blocker, and that dopaminergic stimulation is involved in the diuresis caused by butoxamine, a beta2-blocker. Propranolol is similar to butoxamine, and partially similar to practolol.

Animals↗
PubMed1982

Renal effects of pinane-thromboxane A2 and indomethacin in saline volume-expanded spontaneously hypertensive rats.

In 6-week old spontaneously hypertensive rats (SHR), indomethacin (5 mg/kg i.v.) and pinane-thromboxane A2 (PTA2) (50 micrograms/kg per h i.v.) a thromboxane A2 (TXA2) antagonist as well as a TXA2 synthetase inhibitor, resulted in natriuresis accompanied by an increase in p-aminohippuric acid and inulin clearances. Indomethacin acted as an antidiuretic in 6 week Wistar-Kyoto rats (WKY). PTA2 did not alter renal functions in either 6 week WKY and 18 week SHR. Basal urinary excretion of TXB2 (UTXB2V) was greater in 6 week SHR than in 6 week WKY and 18 week SHR, and that of 6-keto-PGF1 alpha (U6-keto-PGF1 alpha V) did not differ among these strains. Thus, U6-keto-PGF1 alpha V/UTXB2V was lower in the 6 week SHR. Basal urinary excretion of PGE (UPGEV) was much greater in 18 week SHR than in the 2 other groups. In the 6 week SHR, PTA2 decreased UTXB2V and increased U6-keto-PGF1 alpha V without affecting UPGEV, and indomethacin reduced UTXB2V more markedly than did U6-keto-PGF1 alpha V and UPGEV. Thus, both PTA2 and indomethacin increased U6-keto-PGF1 alpha V/UTXB2V in the 6 week SHR. These findings indicate that a disequilibrium in the biosynthesis of vasoconstrictive TXA2 and of vasodilator PGI2 may be involved in water and sodium retention in SHR during the developmental phase of hypertension.

Animals↗
PubMed1983

Interorgan relationships of alanine and glutamine during fasting in the conscious dog.

This study was designed to assess the interorgan relationships of glutamine and alanine in the conscious, overnight fasted dog, and to determine changes which occur with progressive fasting. Dogs were fasted for 18 hr (n = 6), 48 hr (n = 6), and 96 hr (n = 6) prior to the study. Catheters had been previously implanted in the femoral artery, renal vein, portal vein, and hepatic vein, and were used for blood sampling at 30-min intervals during the 3-hr experimental period. Hepatic and renal blood flows were determined by indocyanine green and para-aminohippuric acid (PAH) extraction methods, respectively. Balance data (micromoles/kilogram/minute) were estimated by multiplying the appropriate arteriovenous concentration differences by blood flows. Hepatic uptake of glutamine decreased 50% after a 48-hr fast, and by 96 hr, the liver became a net producer of glutamine. Gut utilization remained constant throughout fasting. The kidney's utilization gradually increased with fasting. The hepatic extraction of alanine fell with fasting, declining to 40% of its original uptake at 96 hr. The gut's production of alanine fell during the first 48 hr of fasting, but remained stable thereafter. The kidney's production of alanine increased throughout the period of starvation. The arterial concentration of glutamine rose with fasting, while that of alanine fell even with a 48 hr fast. The liver, by becoming a net producer of glutamine, and the kidney, by increasing its production of alanine, decrease demands for peripheral release of these two amino acids, and thus may have protein-sparing actions during fasting.

Alanine↗
PubMed1988

Renal effects of low-dose aminophylline and enprofylline in newborn rabbits.

Renal function was studied in 15 newborn New Zealand rabbits administered either 0.6 mg/kg enprofylline intravenously. Each animal acted as its own control. Glomerular filtration rate (GFR) and renal blood flow (RBF) were assessed by the clearances of inulin and para-aminohippuric acid, respectively. Enprofylline, a xanthine with low adenosine antagonistic properties, did not modify urine flow rate, GFR, RBF, renal vascular resistance, filtration fraction, sodium and potassium urinary excretion, whereas administration of theophylline, a potent adenosine antagonist, was associated with a significant increase in diuresis, renal vascular resistance and filtration fraction. The differences observed in the renal effects of theophylline and enprofylline strongly support the view that 1) the renal actions of micromolar concentrations of theophylline are mediated by an antagonism with endogenous renal adenosine; 2) renal adenosine could play a physiological role in the regulation of renal hemodynamics.

Aminophylline↗
PubMed1992

Renal effects of dopamine and dopexamine in the newborn anesthetized rabbit.

The renal effects of dopexamine, a new dopaminergic agonist with marked beta 2-adrenergic agonist properties, but no alpha-adrenergic effect, has been studied in 8 newborn New Zealand rabbits, whose renal functional characteristics show close similarities with those of premature infants. Six animals were used as controls. After a control period, dopexamine was infused intravenously at a rate of 4 micrograms/kg per min and after a wash-out period, at 10 micrograms/kg per min. The renal effects of dopamine were studied in similar conditions. Glomerular filtration rate (GFR) and renal plasma flow (RPF) were determined by inulin and para-aminohippuric acid clearances, respectively. Dopexamine, 4 micrograms/kg per min, did not induce changes in cardiovascular and renal hemodynamics or in renal functions. At 10 micrograms/kg per min, a significant increase in urine flow rate (25 +/- 5%; p less than 0.01), urine sodium excretion (77 +/- 17%; p less than 0.01) and fractional sodium excretion (69 +/- 25%; p less than 0.05) was observed. The GFR, RPF and renal vascular resistance (RVR) were not affected. Heart rate increased slightly but significantly (8 +/- 3%; p less than 0.05), without change in mean blood pressure (MBP). Dopamine, 4 micrograms/kg per min, decreased slightly albeit significantly MBP (3 +/- 1%; p less than 0.05). At 10 micrograms/kg per min the only renal effect was a significant increase in RVR (19 +/- 6%; p less than 0.02). The different actions of these two dopaminergic agonists in this immature model could be explained by their respective ability to activate electively the adrenergic and dopaminergic peripheral receptors. The natriuretic and diuretic effect of dopexamine in normal immature rabbits, in the absence of changes in RPF or GFR is probably mediated by a direct action of this agent on dopaminergic tubular receptors. Failure of these two drugs to increase RPF may be related to an immaturity of the dopaminergic vascular receptors.

Adrenergic Agonists↗
PubMed1995

Protection from hypoxemic renal dysfunction by verapamil and manganese in the rabbit.

The ability of calcium channel blockers to prevent and/or to reverse the hypoxemia-induced renal dysfunction was studied in anesthetized and mechanically-ventilated rabbits. Renal blood flow (RBF) and glomerular filtration rate (GFR) were determined by para-aminohippuric acid and inulin clearance, respectively. Each animal was considered as its own control. In 9 rabbits (group 1), verapamil infusion, 1 microgram.kg-1.min-1, did not change basal renal hemodynamics. In a second group (n = 9), hypoxemia induced marked significant decreases in GFR, RBF and urine flow rate (-22 +/- 5%, -18 +/- 6% and -34 +/- 7% respectively). The administration of verapamil partially reversed the hypoxemia-induced renal dysfunction. Likewise, hypoxemia did not induce any change in renal function in verapamil pretreated rabbits (n = 8). This study shows that verapamil is able to prevent and to partially reverse the adverse effects of hypoxemia on renal hemodynamics. The intrarenal infusion of manganese chloride, another calcium channel blocker, was also effective in blunting the hypoxemia-induced changes in the left infused kidney, but not in the contralateral kidney. The overall results demonstrate that a significant protection from hypoxemic renal dysfunction can be achieved by inhibitors of calcium ion transport.

Animals↗
PubMed1985

Cadmium-induced hepatic and renal injury in chronically exposed rats: likely role of hepatic cadmium-metallothionein in nephrotoxicity.

Rats were injected sc with 0.5 mg Cd/kg, 6 days/week, for up to 26 weeks. Hepatic and renal function and tissue Cd and metallothionein (MT) content were determined in tissues and plasma at various times after Cd injection. Cd in liver and kidney increased linearly for the first 10 weeks of treatment, but thereafter hepatic concentrations of Cd decreased by 33% whereas the content of Cd in kidney remained constant. MT in liver and kidney increased linearly during the first 12 weeks of Cd treatment to 4400 and 2300 micrograms MT/g, respectively, but rose only slightly thereafter. Circulating concentrations of MT progressively increased beginning 2 weeks after Cd treatment and were approximately 10 times control values in rats dosed with Cd for 12 or more weeks. Plasma activities of alanine and aspartate aminotransferase exhibited a time course similar to that observed with MT, and were elevated as early as the sixth week of Cd exposure. Sharp increases in activities of these enzymes also occurred after 10 to 12 weeks of dosing. Hepatic microsomal metabolism of benzo[a]pyrene and ethylmorphine was severely attenuated beginning 4 weeks after Cd. Renal injury occurred after hepatic damage, as evidenced by decreased in vitro p-aminohippuric acid uptake beginning 8 weeks after exposure. Urine outflow increased threefold 11 weeks after Cd exposure began, while urinary protein and Cd excretion increased beginning at Week 9. These data indicate the liver is a major target organ of chronic Cd poisoning, and suggest that Cd-induced hepatic injury, via release of Cd-MT, may play an important role in the nephrotoxicity observed in response to long-term exposure to Cd.

Animals↗
PubMed1989

Renal glutathione depletion and nephrotoxicity of cadmium-metallothionein in rats.

Renal glutathione (GSH) concentrations were reduced approximately 80% at 4 hr after a single injection of buthionine sulfoxime (BSO) (4 mmol/kg body wt) and remained reduced for at least 16 hr in male rats. Following BSO injection, rats were injected with a nephrotoxic dose of cadmium-metallothionein (Cd-MT) (0.3 mg Cd as Cd-MT/kg body wt) and killed 1, 4, or 12 hr later. Damage to the kidney was assessed histologically and by measurement of p-aminohippuric acid (PAH) uptake into renal cortical slices. Although the renal accumulation of Cd following Cd-MT injection was significantly lower in BSO-pretreated rats as compared to nonpretreated rats, the damage to kidney was more severe. At 4 and 12 hr, both Cd-MT-induced inhibition of PAH uptake and morphological damage were significantly increased in BSO-pretreated rats. In certain experiments, the induction of renal intracellular MT synthesis by zinc pretreatment slightly decreased the renal toxicity of Cd-MT in the BSO-treated rats. The results demonstrate that although GSH depletion decreases the renal accumulation of Cd in rats injected with Cd-MT, the nephrotoxicity of Cd-MT is increased. Preinduction of MT in the kidney can only partially overcome this increase in toxicity. Therefore both GSH and intracellular MT levels can influence the renal toxicity of injected Cd-MT.

Animals↗
PubMed1980

Pressure effects of urinary reflux studied with renal autotransplantation and pyelocystostomy.

The pressure effects of urinary reflux on renal structure and function were studied using a canine model in which the kidney was autotransplanted to the iliac fossa and the urine drained through a pyelocystostomy. This provided grade III reflux of urine (distention of the renal pelvis and calyces). A control group of nonrefluxing animals with the ureter and ureterovesical valve intact was studied in an identical fashion, and all animals were observed for one year. The reflux of sterile urine was not associated with any impairment of the inulin clearance or transport maximum of para-aminohippuric acid. There were no histologic abnormalities of glomeruli, tubules, or interstitium noted in the animals exposed to sterile reflux, nor were any differences found between the study and control groups. The transmission of bladder pressures into the renal pelvis and calyces during reflux is considered an unimportant factor in explaining the renal damage noted from sterile reflux of short duration in adults. The pyelocystostomy provides a satisfactory means of urinary drainage, and may be used effectively to study the properties of urinary reflex.

Animals↗
PubMed1995

Antioxidants attenuate endotoxin-induced acute renal failure in rats.

Acute kidney dysfunction, manifested by a reduction in renal blood flow and in the glomerular filtration rate, is a common finding in septic shock. The pathogenetic mechanisms responsible for the renal dysfunction observed in the endotoxemic murine model are not completely understood. In this study, an attempt was made to halt the progressive renal dysfunction in the rats by administration of the antioxidants dimethylthiourea (DMTU) (50 mg/100 g) and superoxide dismutase (SOD) (0.4 mg/100 g) before endotoxin infusion (0.5 mg/100 g), or by inducing endotoxin tolerance. Renal function, assessed by creatinine, inulin, and p-aminohippuric acid clearance, nicotinamide adenine dinucleotide, and electrolyte reabsorption, was measured 4 hours after the endotoxin infusion. Renal function declined in all rats throughout the study period. However, the reduction in renal function was markedly slower in endotoxemic rats administered DMTU and SOD compared with untreated rats. Similar results were found following induction of endotoxin tolerance. These data suggest that DMTU, SOD, and endotoxin tolerance may be potentially beneficial in halting progressive renal damage associated with endotoxemia.

Acute Kidney Injury↗
PubMedDate not supplied

Effect of halogenated vinyl cysteine conjugates on renal tubular active transport.

Addition of halogenated vinyl cysteine conjugates to isolated rabbit kidney tubule suspensions resulted in a decrease in the active transport of para-aminohippuric acid (PAH) and tetraethylammonium bromide (TEA). At 10(-5) M vinyl cysteine conjugate, tubule to medium accumulation ratios (T/M) were similar to those of controls while at 10(-3) M the T/M values decreased to 1, indicating complete inhibition of active accumulation of PAH or TEA. The decreased active transport was not caused by inhibition of mitochondrial oxidation since incubations in the presence of 10(-3) M halogenated vinyl cysteine did not inhibit tubule O2 utilization or production of 14CO2 from [14C]glucose or [14C]succinate. A mechanism is proposed whereby toxicity may result from covalent binding of an active intermediate, produced by enzyme cleavage, to membrane associated nucleophilic groups thereby decreasing active transport.

Animals↗
PubMed1990

The interactions of cis-diamminedichloroplatinum with metallothionein and glutathione in rat liver and kidney.

The involvement of metallothionein (MT) in the nephrotoxicity of cis-diamminedichloroplatinum (c-DDP) was investigated in rats using enzyme excretion and histology as indicators of renal damage. In addition, the effects of renal glutathione (GSH) depletion on the nephrotoxicity of c-DDP was assessed by organic anion transport in renal cortical slices. A dose of 6.0 mg c-DDP/kg body wt, i.p. was administered to rats either as a single injection of 6.0 mg/kg or as six daily injections of 1.0 mg/kg. Concentrations of platinum (Pt) after c-DDP injection in both dosing regimens were approximately 12 micrograms/g in kidney and 2 micrograms/g in liver. However, there were no increases in either hepatic or renal concentrations of MT after both series of c-DDP injections. Fractionation of kidney cytosols from c-DDP injected rats on Sephadex G-75 columns revealed that 60-70% of cytosolic Pt was associated with proteins of high molecular weight and 15-20% of the Pt associated with the low molecular weight ligands. No discernable Pt peak was detected in the elution volume of MT. Pretreatment of rats with ZnSO4 increased both hepatic and renal concentrations of MT, but there was no Pt associated with the MT fraction after a subsequent injection of c-DDP. Small increases in the urinary excretion of the lysosomal enzyme, N-acetyl-beta-D-glucosaminidase and two brush border enzymes, alkaline phosphatase and gamma-glutamyltranspeptidase were observed 2 and 3 days after a single injection of c-DDP (6.0 mg/kg body wt, i.p.). Urinary creatinine excretion decreased by 50% 1 day after c-DDP injection and continued to decrease for the next 2 days. On the third day after c-DDP treatment, a small but significant decrease in body weight was also observed in the c-DDP injected animals. Pretreatment with Zn did not alter the c-DDP-induced enzymuria or renal tubular damage but slightly attenuated both the decrease in creatinine excretion and the loss in body weight. Uptake of the organic anion, p-aminohippuric acid (PAH) was reduced at 12 and 24 h after c-DDP injection. Reduction of tissue GSH concentrations by pretreatment with buthionine sulfoxime (BSO), resulted in only a slight increase in the c-DDP-induced inhibition of PAH uptake at 24 h after c-DDP injection. These results suggest that, in rats, neither MT nor GSH appear to play major roles in the binding or nephrotoxicity of c-DDP.

Acetylglucosaminidase↗
PubMed1989

Potential involvement of renal transport mechanisms in nephrotoxicity.

Among the various physiological factors involved in the development of a nephrotoxic insult, certain renal transport systems may be important. The movement of exogenous organic anions and cations from the blood to the tubular fluid is well recognized. The anion transport system, which has been extensively characterized for the transport of p-aminohippuric acid, may have particular relevance. The nephrotoxic effect of citrinin, certain cephalosporin antibiotics and cysteine conjugates in rats and in isolated renal cells can be blocked by probenecid, a drug known to block the organic anion transporter competitively. The reduction in toxic response is correlated with the renal and cellular content of the nephrotoxic chemical.

Animals↗
PubMed1993

Measurement of total and unilateral renal blood flow by oblique-angle velocity-encoded 2D-cine magnetic resonance angiography.

Two independent measurements of total renal blood flow (RBF) were made in healthy human subjects (n = 14, mean age 30 yr) by CINE phase-contrast magnetic resonance angiography. RBF, measured by summing the flows measured in the right and left renal arteries, was 1152 +/- 44 ml/min (mean +/- SE). RBF, measured from the difference between supra- and infrarenal abdominal aorta flow, was 1109 +/- 68 ml/min. Regression analysis of the comparison of these two different RBF calculations yielded a correlation coefficient of 0.72 at a p < .05 level of significance. Based on other studies of RBF in normal subjects by para-aminohippuric acid (PAH) clearance, the expected RBF in this subject group was 1211 +/- 62 ml/min. The results indicate that noninvasive measurement of RBF is possible using phase-contrast magnetic resonance methods.

Adolescent↗