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PubMed1986

Transport of cimetidine by the rat choroid plexus in vitro.

To characterize the transport system of cimetidine, an organic cation, in the blood-cerebrospinal fluid barrier, the accumulation of cimetidine by the isolated rat choroid plexus was examined. Accumulation of cimetidine was against a concentration gradient via a saturable process (Km = 53 microM, Vmax = 12 nmol/ml/min) that was inhibited by sulfhydryl reagents (p-hydroxymercuribenzoate), metabolic inhibitors (KCN and 2,4-dinitrophenol) and hypothermia (Q10 = 4.5), but did not require inward Na+ gradient. Organic cations such as 1N-methylnicotinamide, tetraethylammonium, choline, histamine and creatinine did not affect the accumulation of cimetidine at the concentration of 1 mM. Cimetidine did not affect the accumulation of tetraethylammonium. More lipophilic cations such as quinidine and quinine inhibited not only the accumulation of cimetidine but also that of an organic anion, benzylpenicillin, although the inhibitory mechanisms are not known. One millimolar of organic anions, such as 5-hydroxyindoleacetic acid, p-aminohippuric acid, homovanillic acid, salicylic acid and benzylpenicillin, inhibited the accumulation of cimetidine. Furthermore, the accumulation of organic anions (benzylpenicillin and salicylic acid) showed saturability and was inhibited by cimetidine. Cimetidine and the organic anions thus showed a mutual inhibition. Oligopeptides also inhibited the accumulation of cimetidine. These findings suggested that cimetidine transport in the choroid plexus is via carrier-mediated active transport process, but does not require inward Na+ gradient. This transport is inhibited by several compounds with different properties like oligopeptides, lipophilic cations and organic anions, although the inhibitory mechanism is not known.

Amino Acids↗

PubMedDate not supplied

High performance liquid chromatographic characterisation and quantitation of p-aminobenzoic acid N-acetylation in Chinese subjects.

p-Aminobenzoic acid (PABA), p-acetamidobenzoic acid (PADB) and p-aminohippuric acid (PAH) have been separated and determined by a reversed phase, isocratic high performance liquid chromatographic (HPLC) procedure simultaneously. The mobile phase, at 1.5 ml min-1, used was 10 mM sodium hydrogen phosphate buffer, pH 3.5, containing 40% methanol. The eluent was detected at 270 nm. Linear relationship was obtained from 0 to 2.0 micrograms ml-1 of each compound with the corresponding peak-height ratio using p-methylamino-benzoic acid (PMAB) as the internal standard. Urine samples were obtained from healthy Chinese volunteers after oral dosing of 200 mg PABA which was used as a model substance for metabolic investigation of N-acetylation and other conjugation reactions. The 24 hour urinary recovery, from 43 healthy subjects, of PABA, PABA-COOH conjugates, PADB and PADB-COOH conjugates were (mean +/- S.D.) 2.9 +/- 1.5%, 5.2 +/- 3.3%, 13.9 +/- 4.0% and 42.9 +/- 9.8% of the ingested dose respectively. These accounted for 64.9 +/- 12.0% of total dose ingested in 24 hour. In contrast to previously reported findings on one Caucasian subject, no PAH was identified in the urine, and N-acetylation was the major route of metabolism of PABA apart from conjugation at the -COOH group in this group of Chinese volunteers. It is proposed that PABA metabolism may be a useful probe to study ethnic and geographic variation in N-acetylation.

4-Aminobenzoic Acid↗

PubMed1990

Effect of furegrelate on renal plasma flow after angiotensin II infusion.

We had previously shown that selective thromboxane synthetase inhibition with furegrelate increases urinary excretion of 6-ketoPGF1 alpha, the hydrolysis product of prostacyclin after stimulation of renal prostaglandin synthesis with furosemide. The present study assessed the functional significance of this "redirection" of prostaglandin formation using a more physiologic stimulus, angiotensin II. Sprague-Dawley rats (n = 27) were fitted with a transabdominal bladder cannula. Five days later they were given angiotensin II (10 mg.kg-1.min-1) by intravenous infusion. After 30 min, an infusion of furegrelate, 2 mg/kg, then 2 mg.kg-1.h-1, (n = 9); indomethacin, 2 mg/kg, then 2 mg.kg-1.h-1 (n = 9); or vehicle, 250 microL, then 0.018 mL/min (n = 9) was begun for 60 min. Clearance of [14C]para-aminohippuric acid was taken as a measure of renal plasma flow. Angiotensin II raised the mean arterial pressure in all groups. Administration of furegrelate or indomethacin did not change mean arterial pressure or heart rate. Angiotensin II reduced [14C]p-aminohippuric acid clearance by about 32% (1.42 +/- 0.18 to 0.97 +/- 0.07 mL.min-1.100 g-1, p less than 0.05). Furegrelate attenuated this renal vasoconstriction (0.97 +/- 0.07 to 1.38 +/- 0.17 mL.min-1.100 g-1, p less than 0.05), while indomethacin increased it by a further 32% (1.78 +/- 0.12 to 1.20 +/- 0.12 mL.min-1.100 g-1, p less than 0.05). Vehicle alone had no effect. Furegrelate reduced serum thromboxane B2 by 90% (6.52 +/- 0.030 to 0.7 +/- 0.21 ng/100 microL, p less than 0.05), while indomethacin reduced it by 73% (5.9 +/- 0.99 to 1.4 +/- 0.20 ng/100 microL, p less than 0.05). We conclude that furegrelate attenuates the renal vasoconstriction of angiotensin II, presumably by enhancing the formation of vasodilator prostaglandins.

Angiotensin II↗

PubMed2003

Dendrimers conjugates for colonic delivery of 5-aminosalicylic acid.

The water-soluble polyamidoamine (PAMAM) dendrimer conjugates for colonic delivery of 5-aminosalicylic acid (5-ASA) were designed. The drug was bound to the dendrimer using two different spacers containing azo-bond, p-aminobenzoic acid (PABA) and p-aminohippuric acid (PAH). Incubation of PAMAM dendrimer conjugates containing PABA and PAH spacers with rat cecal contents at 37 degrees C gradually released 5-ASA with time and the amount of drug released was 45.6 and 57.0% of the dose in 24 h, respectively. The release of the drug from the commercial prodrug, sulfasalazine was significantly faster than both conjugates (80.2% of the dose in 6 h). No 5-ASA was detected from the incubation of dendrimer conjugates with the homogenate of the stomach or phosphate buffer, pH 1.2 and 6.8. Only a small amount of 5-ASA was found after incubation of both conjugates with the homogenate of the small intestine for 12 h. It appears that this PAMAM dendrimer can be developed for use as a carrier for colon-specific drug delivery.

4-Aminobenzoic Acid↗

PubMed1983

Chronic local infusion into the renal artery of unrestrained rats.

A method is described for providing chronic access to the right renal artery of unrestrained rats. It consists of insertion of a very thin (OD 0.2 mm) catheter into the right suprarenal artery of Wistar rats. The suprarenal artery originates from the right renal artery. After the cannula has been guided subcutaneously to the neck, it is connected to an Alzet osmotic minipump. The method has a success ratio of over 90% for periods up to 14 days. In the present study, we investigated the effects of catheter implantation on renal hemodynamics in uninephrectomized rats that were infused with saline for 2, 6, or 14 days. Values were compared with those obtained in control rats. Glomerular filtration rate (GFR) and effective renal plasma flow (ERPF) were estimated from plasma clearances of 51Crethylenediaminetetraacetic acid and 125I-p-aminohippuric acid, respectively. Mean arterial pressure was between 107 +/- 2 and 116 +/- 2 mmHg in all animals. Neither GFR nor ERPF was influenced by catheter implantation. It is concluded that the method does not interfere with renal function.

Animals↗

PubMed1993

Rabbits with a genetic impairment in baroreceptor reflex sensitivity show abnormal renal haemodynamics and proximal tubular sodium reabsorption in response to a saline infusion.

OBJECTIVE: To compare renal haemodynamics and proximal tubular sodium reabsorption (PTSR) in response to an acute intravenous saline infusion in rabbits bred for genetic differences in cardiac baroreflex sensitivity (BRS). Rabbits with low BRS increase their blood pressure significantly on a high-salt diet, in association with an initial delay in sodium excretion. It was hypothesized that this could occur through an impaired baroreflex regulation of renal sympathetic nerve activity. This, in turn, would alter renal blood flow and PTSR. DESIGN: Experiments were performed in two groups of normotensive male rabbits (n = 10 per group), one of which had high BRS (> 5 beats/min per mmHg; group I) and one of which had low BRS (< 4 beats/min per mmHg; group II). Effective renal plasma flow (ERPF) was measured by para-aminohippuric acid clearance, and PTSR by the lithium clearance technique. Sodium, lithium, para-aminohippuric acid and glomerular filtration rate were measured from urine samples collected every 30 min (for 90 min) via an indwelling bladder catheter, during a control infusion of glucose (30 mg/ml) NaCl (1.8 mg/ml), and for 2 h after a threefold increase in NaCl. RESULTS: Group I rabbits increased their ERPF by approximately 40%, in response to saline, and doubled their sodium and lithium clearances within the 2 h, but those in group II did not change their cation excretion or their ERPF significantly during this period. Blood pressure did not increase in either group. CONCLUSIONS: A genetic impairment in BRS may be responsible for the inadequate depression of renal sympathetic nerve activity, which results in a failure to increase ERPF and suppress sodium reabsorption in the proximal tubule in response to salt loading.

Absorption↗

PubMed1976

Renal extraction of gentamicin in anesthetized dogs.

The tubular handling of gentamicin (G) and its intrarenal distribution were determined to elucidate the mechanism of G accumulation in the kidney. At a serum level of 11.1 +/- 0.5 mug/ml (10 animals), as maintained by constant infusion for 5 h, serum Na(+) and K(+), arterial pressure, effective renal plasma flow and glomerular filtration rate remained undisturbed. The clearance values in milliliters per minute for G, inulin, and p-aminohippuric acid were 40.3 +/- 1.8, 49.9 +/- 2.8, and 132 +/- 14, respectively. The ratio of clearance of G to clearance of inulin was 0.82 +/- 0.04 (P < 0.005), suggesting net reabsorption of G by the renal tubules. The renal cortex/serum ratio for G was 11.9 +/- 2.1, and the medulla/serum ratio was 2.7 +/- 0.4, indicating greater uptake of G by the cortex. The extraction ratio of p-aminohippuric acid was 0.74 +/- 0.03. In contrast, the extraction ratio of G was 0.20 +/- 0.03, which was significantly lower than that of inulin (0.30 +/- 0.04). It is concluded that the accumulation of G in the cortex was due to tubular reabsorption. Probably some of the reabsorbed G became trapped in the epithelial cells after crossing the luminal membrane, whereas some returned to the circulation.

Animals↗

PubMedDate not supplied

Differential renal handling of angiotensin-converting enzyme inhibitors enalaprilat and lisinopril in rats.

Enalaprilat, the active metabolite of enalapril, and its lysine analogue lisinopril are potent nonsulfhydryl angiotensin-converting enzyme inhibitors. Earlier studies from our laboratories demonstrated that neither drug is significantly metabolized, and both are almost exclusively eliminated by renal excretion. This report compares the renal excretory mechanisms for these structurally related compounds in the rat. After an iv, 1-mg/kg dose, ratios of renal clearance (CLR) of unbound drug to glomerular filtration rate (GFR) for enalaprilat and lisinopril were 2.72 +/- 0.70 and 1.01 +/- 0.18, respectively, suggesting that enalaprilat, but not lisinopril, was actively secreted by the kidneys. Treatment with probenecid and p-aminohippuric acid, potent competitive inhibitors for the renal anionic transport system, caused a profound decrease in the renal clearance of enalaprilat to the level of GFR. The CLR/fu.GFR, where fu is the unbound fraction, became 1.10 +/- 0.09 and 1.25 +/- 0.25, respectively. These results and the fact that quinine, a potent inhibitor for the cationic transport system, had little effect on the renal clearance of enalaprilat indicated that enalaprilat is secreted by the organic anion transport system. On the other hand, probenecid, p-aminohippuric acid, and quinine had no effect on the renal clearance of lisinopril, suggesting that lisinopril is eliminated exclusively by glomerular filtration.

Angiotensin-Converting Enzyme Inhibitors↗

PubMed1990

Altered renal function in broilers during aflatoxicosis.

Experiments were conducted to determine the effects of aflatoxicosis on acid-base balance, urine flow rate (V), glomerular filtration rate (GFR), clearance of para-aminohippuric acid (CPAH), plasma osmolality, and the renal handling of Na, K, Ca, and P. Three-week-old broilers were gavaged with aflatoxin at a dose of 2 mg/kg of BW per day for 10 consecutive days. Control birds received an equal volume of corn oil, the aflatoxin carrier vehicle. On the eleventh day, the birds were anesthetized and prepared for renal function analysis. A solution containing inulin, para-aminohippuric acid, and mannitol was infused at a low infusion rate (.1 mL/kg of BW per min) and a high infusion rate (.4 mL/kg of BW per min) to determine if aflatoxin affects the renal response to an acute volume load. Aflatoxicosis decreased the fractional excretion of phosphorous (FEP) and plasma Ca concentration but did not significantly alter any other renal function or acid-base variables. The decrease in FEP and plasma Ca may be a direct result of renal tubular damage, decreased Ca absorption from the gut, or a result of altered circulating levels of parathyroid hormone (PTH), and possibly decreased renal sensitivity to PTH.

Animals↗

PubMed1981

Peritubular interaction of unconjugated bilirubin in isolated perfused rat kidney.

1. The interaction of unconjugated bilirubin with peritubular cell membranes of the rat kidney was studied by means of an isolated rat-kidney preparation applying the multiple-indicator-dilution technique. 2. Inulin was used as an extracellular marker and p-aminohippuric acid as a model of organic anion that interacts with the peritubular membrane. 3. A single renal artery injection of a mixture containing inulin and unconjugated bilirubin was followed by the appearance of the two compounds in the venous effluent. The unconjugated bilirubin curve was always under the curve of inulin and its mean transit time was always less than that of inulin. 4. The cumulative venous recovery of inulin was higher than that of unconjugated bilirubin. 5. When unconjugated bilirubin uptake was plotted against the injected dose of pigment the relationship suggested a saturation phenomenon. 6. The recovery of p-aminohippuric acid was significantly increased when unconjugated bilirubin was added. 7. The results provide evidence for the interaction of unconjugated bilirubin with the peritubular cell membranes of rat kidney.

Animals↗

PubMed1985

Functional role of thromboxane production by acutely rejecting renal allografts in rats.

We investigated the role of thromboxane in mediating the reduction in renal function and renal blood flow characteristic of acute renal allograft rejection. We transplanted kidneys from Lewis rats to Brown-Norway recipients. By the third day after transplantation, histologic changes that were consistent with cellular rejection occurred in the kidney. These changes were associated with a moderate reduction in renal function. By day 6, histologic changes of rejection were advanced and included interstitial and perivascular infiltration by mononuclear cells. The clearances of inulin and para-aminohippuric acid were also markedly reduced. As renal function deteriorated, thromboxane B2 (TXB2) production by ex vivo perfused renal allografts increased progressively from 2 to 6 d after transplantation. However, prostaglandin (PG) E2 and 6-keto PGF1 alpha production remained essentially unchanged. There was a significant inverse correlation between the in vivo clearance of inulin and the log of ex vivo TXB2 production. Infusion of the thromboxane synthetase inhibitor UK-37248-01 into the renal artery of 3-d allografts significantly decreased urinary TXB2 excretion and significantly increased renal blood flow (RBF) and glomerular filtration rate (GFR). Although renal function improved significantly after the acute administration of UK-37248-01, GFR and RBF did not exceed 33 and 58% of native control values, respectively. In other animals, daily treatment with cyclophosphamide improved the clearances of inulin and para-aminohippuric acid and reduced thromboxane production by 6-d renal allografts. These studies demonstrate that histologic evidence of rejection is associated with increased renal thromboxane production. Inhibition of thromboxane synthetase improves renal function in 3-d allografts. Cytotoxic therapy improves renal function, reduces mononuclear cell infiltration, and decreases allograft thromboxane production. Thus, the potent vasoconstrictor thromboxane A2 may play a role in the impairment of renal function and renal blood flow during acute allograft rejection.

Animals↗

PubMed1986

Kinetic evidence for a common transport route of benzylpenicillin and probenecid by freshly prepared hepatocytes in rats. Influence of sodium ion, organic anions, amino acids and peptides on benzylpenicillin uptake.

Hepatic transport system of benzylpenicillin was characterized by using freshly prepared rat hepatocytes. Uptake of benzylpenicillin and cefpiramide did not require the presence of sodium ion in the incubation medium. No influence of several kinds of amino acids (leucine, histidine, phenylalanine, valine, alanine, glutamic acid and glycine) and peptides (prolyl-leucine, glycyl-glycine, glycyl-sarcosine, glycyl-leucine and gamma-glutamyl-cysteinylglycine) was observed for benzylpenicillin uptake into hepatocytes. Taurocholic acid and cholic acid significantly inhibited benzylpenicillin uptake. The kinetic study revealed that taurocholic acid inhibited benzylpenicillin uptake in a noncompetitive fashion. A similar effect of benzylpenicillin on taurocholic acid uptake was observed, suggesting that the affinity site of the hepatic transport carrier of benzylpenicillin is distinct from that of taurocholic acid. It is noteworthy that p-aminohippuric acid and p-acetylaminohippuric acid did not inhibit benzylpenicillin uptake. In contrast to the mutual inhibition behavior of benzylpenicillin and taurocholic acid, benzylpenicillin is fully and competitively inhibited by the simultaneous addition of probenecid. The inhibition constant Ki value of probenecid was calculated to be 0.322 mM. The uptake of probenecid was also significantly inhibited by benzylpenicillin. It is postulated that the affinity site of benzylpenicillin transport carrier is the same as that of probenecid and that the whole process of the benzylpenicillin transport system is common, at least in part, to the probenecid transport process in the liver.

Amino Acids↗

PubMed1976

Modification of in vivo lacrimal gland secretion by 2,4-dinitrophenol.

Mecholyl-stimulated flow from the excretory duct of the rabbit lacrimal gland in vivo was recorded continuously and samples of Mecholyl-stimulated fluid were collected before, during, and after 30 min of local intra-arterial infusion of 2,4-dinitrophenol (DNP). Compared with the control period, Mecholyl-stimulated flow during the DNP infusion was 60-70% less; [K+] was the same and [Na+] and [Cl-] were higher in the Mecholyl-stimulated fluid. The changes that occurred during the DNP infusion were not produced by infusion of the solvent (NaHCO3) or an acid with similar pK (para-aminohippuric acid) nor were the changes related to any effect of DNP on the general circulation. The magnitude of the changes during the DNP infusion increased as the dose of DNP increased and the inhibition of flow changes in [Na+] and [Cl-] during the DNP infusion were reversible. The results are compatible with the hypothesis that stimulation by Mecholyl involves oxidative metabolsim at the duct level but they do not exclude the possibility that oxidative metabolism may also be involved in formation of the primary fluid at the acinar level.

Aminohippuric Acids↗

PubMed1997

Nitrogen balance in adult female mink (Mustela vision) in response to normal feeding and short-term fasting.

Ten adult female mink (Mustela vison) were studied in a 7 d balance experiment consisting of a 2 d pre-surgery feeding period, followed by surgery, 1 d of recovery 4 d of ad libitum feeding, and a 2 d fasting period. In this experiment (Expt A) the animals had osmotic pumps implanted for continuous release of radioactively-labelled p-aminohippuric acid (p-aminobenzoyl-2-[3H]glycine; [3H]PAH; n 10) and 14C-labelled inulin ([14C]IN; n 5). Repeated 24 h collections of urine, corrected to 100% [3H]PAH or [14C]IN recovery, were used for accurate determination of N balances, 24 h urinary excretion of urea, creatinine, and total N, and calculation of mean 24 h renal clearance rates for endogenous creatinine and inulin. N balances were slightly below zero, but not significantly different between feeding and fasting periods, indicating that correction to 100% [3H]PAH recovery resulted in slight overestimation of the final balances. During fasting, withdrawal of the dietary water and protein loads resulted in a dramatic decline in 24 h urinary volume, and urea and creatinine excretion. Large individual variations in 24 h urinary creatinine excretion (with relative variation coefficients up to 30%) confirmed that this is an unreliable index of the completeness of urine collection. In this respect, recovery rates of [3H]PAH proved far more consistent. Renal clearance values obtained in fed mink were in fair agreement with published data from cats, dogs and ferrets (Mustela putorius furo). Inulin clearance was about 30% higher than endogenous creatinine clearance, although its decline in response to fasting was not significant. In a separate study (Expt B) another ten female mink were equipped with osmotic pumps containing [3H]PAH for determination of 24 h excretion rates of purine derivatives. During feeding, allantoin accounted for more than 97% of the excretion of purine derivatives in urine, uric acid making up less than 2.5%, xanthine and hypoxanthine less than 1%. In fasted animals, urinary excretion of each of these purine derivatives declined to less than 50% of the feeding value. In conclusion, an experimental technique is presented for efficient and accurate measurements of daily urinary excretion of nitrogenous constituents, which allows for correct determination of N balances in adult mink and, presumably, in other mammalian species.

Allantoin↗

PubMed2001

Analytical validation for a series of marker compounds used to assess renal drug elimination processes.

Renal drug elimination is determined by glomerular filtration, tubular secretion, and tubular reabsorption. Changes in the integrity of these processes influence renal drug clearance, and these changes may not be detected by conventional measures of renal function such as creatinine clearance. The aim of the current study was to examine the analytic issues needed to develop a cocktail of marker drugs (fluconazole, rac-pindolol, para-aminohippuric acid, sinistrin) to measure simultaneously the mechanisms contributing to renal clearance. High-performance liquid chromatographic methods of analysis for fluconazole, pindolol, para-aminohippuric acid, and creatinine and an enzymatic assay for sinistrin were developed or modified and then validated to allow determination of each of the compounds in both plasma and urine in the presence of all other marker drugs. A pilot clinical study in one volunteer was conducted to ensure that the assays were suitable for quantitating all the marker drugs to the sensitivity and specificity needed to allow accurate determination of individual renal clearances. The performance of all assays (plasma and urine) complied with published validation criteria. All standard curves displayed linearity over the concentration ranges required, with coefficients of correlation greater than 0.99. The precision of the interday and intraday variabilities of quality controls for each marker in plasma and urine were all less than 11.9% for each marker. Recoveries of markers (and internal standards) in plasma and urine were all at least 90%. All markers investigated were shown to be stable when plasma or urine was frozen and thawed. For all the assays developed, there were no interferences from other markers or endogenous substances. In a pilot clinical study, concentrations of all markers could be accurately and reproducibly determined for a sufficient duration of time after administration to calculate accurate renal clearance for each marker. This article presents details of the analytic techniques developed for measuring concentrations of marker drugs for different renal elimination processes administered as a single dose to define the processes contributing to renal drug elimination.

Adrenergic beta-Antagonists↗

PubMed2005

Transepithelial urate transport by avian renal proximal tubule epithelium in primary culture.

Birds are uricotelic, and because they excrete urate by renal tubular secretion, they provide a convenient model for examination of this process. Primary monolayer cultures of the isolated renal proximal tubule epithelium from the domestic chicken, Gallus gallus L., were mounted in Ussing chambers where several substrates/inhibitors of renal organic anion transporters were tested for the sidedness and specificity of their effects on transepithelial urate transport. Transepithelial electrical resistance, electrical potential and sodium-dependent glucose current were monitored to detect nonspecific effects. Under control short-circuited conditions the ratio of unidirectional fluxes of [(14)C]urate was found to be 3:1. Active net secretion was specifically inhibited by 1 mmol l(-1) probenecid and 10 mmol l(-1) para-aminohippuric acid (PAH). Bromocresol Green, cimetidine, nocodozole, cytochalasin D and ouabain also inhibited secretion but were toxic. Interstitial-side lithium (5 mmol l(-1)) and glutarate (1 mmol l(-1)) specifically blocked transport, but 10-100 micromol l(-1) glutarate had no effect. Interstitial estrone sulfate (ES) stimulated urate secretion at 10 micromol l(-1) but was inhibitory at 500 micromol l(-1). Active PAH secretion (5:1 flux ratio) was inhibited 34% by 330 micromol l(-1) urate. ES (500 micromol l(-1)) blocked the remainder. From the lumen side, glucose-free, Cl(-)-free and high K(+) (30 mmol l(-1)) solutions, or an alkaline pH of 7.7 had no effect on urate transport and neither did several compounds known to be uricosuric. Lumen-side methotrexate (500 micromol l(-1)) and MK571 (20 micromol l(-1)) strongly inhibited urate secretion. MK571 had no effect from the interstitial side. RT-PCR revealed mRNA for OAT1-, OAT3-, MRP2- and MRP4-like organic anion transporters in chicken proximal epithelium.

Animals↗

PubMed1984

Effect of papaverine on organic anion transport in rat kidney cortical slices.

The present studies were conducted to further investigate a role of cyclic nucleotides for organic anion transport in rat kidney cortical slices by using papaverine as a phosphodiesterase inhibitor. Papaverine was chosen for this study because this drug is an organic cation, a transport system of which is thought to be clearly separable from an organic anion transport system. Papaverine inhibited not only p-aminohippuric acid (PAH) accumulation in the slices but also urate one. Pretreatment of the slices with papaverine was effective for significant inhibition of PAH accumulation during subsequent incubation in the absence of papaverine. The present results suggest that a relationship may exist between cyclic nucleotides and organic anion transport in rat kidney cortical slices, although further work is necessary before the above evaluation can be given.

Animals↗

PubMed1981

Renal functional recovery of the hydronephrotic kidney predicted before relief of the obstruction.

Employing technetium labeled dimercaptosuccinic acid, we predicted the inulin and p-aminohippuric acid (PAH) clearances after recovery of an obstructed kidney before relief of the obstruction. Sixteen rabbits had one renal unit obstructed for varying period of time. The animals were scanned immediately before relief of the obstruction. After 4 to 6 months recovery, inulin and PAH clearances were measured in all animals. The scans were mathematically analyzed, and accurately predicted the inulin and PAH clearances obtained after complete recovery (P less than 0.001 and P less than 0.001, respectively). Six rabbits were scanned at the time of the clearance measurements. By a different mathematical analysis, inulin and PAH clearance measured concurrently correlated with the scan (P less than 0.001 and P less than 0.01 respectively).

Animals↗