Organic acid movement out of the central canal.
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Acids↗
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Determination of plasma and tissue levels of tyramine by radioimmunoassay.
Antibodies were prepared against tyramine. The antigen was prepared as follows: p-Aminohippuric acid was coupled to mBSA using a carbodiimide reagent. The amino group was diazotized an attached to the aromatif ring of TYR. The immunogen in Freund's complete adjuvant was injected into rabbits. The specificity of the resulting antibody was determined by radioimmunoassay. Using random-labeled TYR-3H, TYR, its metabolites, phenethylamine analogs, catecholamines, and certain amino acids were evaluated by a competitive binding assay method. With this technique 4 ng of TYR inhibited the binding of TYR-3H by 50%. The radioimmunoassay of TYR was used to measure the plasma, urine, and tissue levels of TYR in rabbits. The plasma disappearance curve of TYR revealed a biphasic pattern with t1/2 of 2 min and 54 min. The highest concentration of TYR was found in adrenals and spleen. The factthat the major metabolites of TYR and a series of pharmacologically important sympathomimetics and catecholamines did not interfere, makes the radioimmunoassay of TYR a useful, simple, sensitive, and spedific method for the direct analysis of TYR in biological meterials.
Animals↗
Effects of ochratoxin A alone and in combination with citrinin on kidney function of single comb White Leghorn pullets.
The present study was designed to evaluate the acute effects of ochratoxin A (OA) on pullet renal function, and to determine if the diuretic effects of citrinin are altered by acute ochratoxicosis. Birds were injected intramuscularly with a 1-mg/mL solution of OA at a dose of 5 mg/kg body weight for 2 consecutive days. Control birds received an equal volume injection of the OA carrier vehicle (100% ethanol). On the 3rd day, birds were anesthetized and prepared for renal function studies. Following 30 min of control urine and plasma collection, an intravenous infusion containing 400 ppm citrinin was initiated, and urine and plasma were collected for an additional 70 min. The OA alone caused an increase in manure moisture and increased hematocrits (hemoconcentration), but direct effects on glomerular filtration rate (GFR), urine flow rate/GFR, para-aminohippuric acid clearance (CPAH), free water clearance (FWC), and electrolye excretion (Na, K, Ca, P) were not consistently demonstrated. The OA may cause hemoconcentration by causing a subtle increase in urine flow (diuresis), or by increasing intestinal water loss (diarrhea). Citrinin infusion caused increased urine flow rate, increased urine flow rate/GFR, increased FWC, increased Na excretion, and decreased urine osmolality. Pretreatment with OA attenuated these effects of citrinin, presumably due to renal compensation for the OA-induced hemoconcentration. Citrinin and OA do not appear to have additive diuretic effects during the first 48 h of toxin exposure.
Animals↗
Effects of chronic ochratoxin A and citrinin toxicosis on kidney function of single comb White Leghorn pullets.
The objectives of the present study were to examine the effects of repeated or chronic ochratoxin A (OA) and citrinin exposure, and to determine if severe ochratoxicosis permanently alters renal function in pullets. The OA-treated birds were injected intramuscularly (breast muscle) with a 1 mg/mL solution of OA at a dose of .25 mg/kg BW or .5 mg/kg BW. Citrinin-treated birds were injected with a 6 mg/mL solution of citrinin at a dose of 6 mg/kg BW. Control birds received an equal volume injection of the citrinin and OA solvent, 100% ethanol, at a dose of 1 mL/kg BW. Kidney function was evaluated after 10 consecutive days of OA, citrinin, or ethanol injection, and 2 wk following the final injections. Venous blood gas measurements were taken after the seventh day of injection. The OA increased urine flow rate, decreased urine osmolality, increased ion excretion (Na, K, Ca, P), increased water consumption, increased manure moisture, and caused a relative alkalosis when measured immediately after 10 days of OA injection. These effects of OA were not detected 2 wk later. Citrinin increased manure moisture, decreased plasma P, increased the clearance of para-aminohippuric acid, and had no consistent effect on blood acid-base parameters. The results suggest that OA may cause an osmotic diuresis by inhibiting tubular reabsorption of electrolytes. The data also suggests that the effects of OA may be reversible simply by discontinuing toxin administration. Although the citrinin-induced increase in manure moisture indicates that citrinin had an effect on renal function, renal function analysis suggests that even repeated exposure to high doses of citrinin may only have a short duration of diuretic action on the kidneys.
Analysis of Variance↗
[Influence of single leaf Asarum himalaicum on renal function of rabbits].
OBJECTIVE: To study the influence of single leaf Asarum himalaicum on the renal function of rabbits. METHODS: Rabbits were divided into three groups. Asarum himalaicum, Asarum heterotropoides and normal saline were intravenously administered to the rabbits of one group respectively. The urine volume per minute, urine pH, urine glucose, protein and red blood cells, BUN, SCr, TXB2, 6-keto-PGF1alpha, TXB2/6-keto-PGF1alpha, endothelin, p-aminohippuric acid clearance rate and phenolsulfonphthalein excretion rate were tested before and after the administration. RESULTS: A certain dosage of single leaf Asarum himalaicum caused acute renal failure in rabbits. The indices tested were significantly different between rabbits administered Asarum himalaicum and normal saline. As compared with the rabbits administered Asarum heterotropoides, the results of indices tested decreased, but without statistical significance, except for SCr. CONCLUSION: The single leaf Asarum himalaicum can cause renal damage to rabbits. Its renal toxicity is lower that that of Asarum heterotropoides.
Animals↗
Is l-arginine infusion an adequate tool to assess endothelium-dependent vasodilation of the human renal vasculature?
Systemic administration of L-arginine alters renal haemodynamics in humans. We examined whether L-arginine-induced vasodilation of the renal vasculature is related to an increased production and release of NO by comparing the effects of L- and D-arginine on renal endothelium-dependent vasodilation. In a double-blind randomized cross-over study including 20 young, healthy male white subjects (age 26+/-2 years), we determined the effects of intravenous administration of L-arginine or its enantiomer D-arginine, at doses of 100 mg/kg body weight for 30 min or 500 mg/kg for 30 min, on renal haemodynamics. Renal plasma flow (RPF) and glomerular filtration rate (GFR) were assessed by a constant-infusion input-clearance technique (using p-aminohippuric acid and inulin respectively). In addition, changes in blood pressure, heart rate, urinary sodium excretion (U(Na)) and urinary cGMP were measured. HPLC was used to determine L- and D-arginine concentrations. Intravenous infusion of L-arginine at 100 mg/kg for 30 min increased RPF from 641+/-87 to 677+/-98 ml/min (P=0.019), whereas infusion of D-arginine did not (from 642+/-74 to 657+/-86 ml/min; not significant). The change in RPF was more marked during the infusion of L-arginine than during the infusion of D-arginine (+36+/-61 versus +16+/-57 ml/min; P=0.037). Infusion of both L- and D-arginine at doses of 500 mg/kg for 30 min increased RPF from baseline [from 641+/-87 to 762+/-133 ml/min (P<0.001) and from 642+/-74 to 713+/-120 ml/min (P=0.004) respectively], but the change in RPF again was greater in response to L-arginine infusion than to infusion with D-arginine (+121+/-97 versus +71+/-94 ml/min; P=0.018). In accordance, changes in renal vascular resistance (RVR) were higher in response to L-arginine compared with D-arginine for both doses (P<0.05 and P<0.001 respectively). U(Na) increased only with L-arginine (change in U(Na), +0.33+/-0.26 mmol/min; P<0.01) but not with D-arginine (change in U(Na), +0.11+/-0.17 mmol/min; not significant). The change in U(Na) was more pronounced during infusion of L-arginine compared with infusion of D-arginine (P=0.023). In parallel, urinary excretion of cGMP only increased in response to L-arginine (+676+/-272 pmol/l; P=0.038) and not during D-arginine infusion (+185+/-153 pmol/l; not significant). L-Arginine-induced changes in RPF, RVR, U(Na) and cGMP excretion differed significantly from those induced by D-arginine. Thus although no direct measurements of NO synthesis were performed, putative markers of NO synthesis suggest that the renal vasodilatory response to L-arginine, at least in part, was due to increased production and release of NO. The dose of L-arginine at 100 mg/kg for 30 min emerged as the most suitable, because of the absence of systemic haemodynamic changes. The effects of infusion of L-arginine at 500 mg/kg for 30 min on renal endothelium-dependent vasodilation need to be corrected for the effects of D-arginine before conclusions can be drawn.
Adult↗
[Effects of intravenous nicardipine, prostaglandin E1, nitroglycerin, sodium nitroprusside, and epidural lidocaine on hepatic and renal blood flow during hypotensive anesthesia].
We studied the effects of intravenous nicardipine (NIC), prostaglandin E1 (PGE1), nitroglycerin (TNG), sodium nitroprusside (SNP) and epidural lidocaine (LID) on hepatic and renal blood flow during general anesthesia (nitrous oxide-oxygen-sevoflurane) in 46 female patients undergoing unilateral total hip arthroplasty. During operations, hepatic blood flow, glomerular filtration rate, renal plasma flow, and renal tubular injury were measured by R 15 ICG (15 minutes retention rate of indocyanine green), CCR (creatinine clearance), CPAH (para-aminohippuric acid clearance), and urinary excretion of NAG and beta 2-microglobulin. Significant elevation of R 15 ICG was observed in the hypotensive state in the TNG group and the elevation of R 15 ICG indicates that blood flow to the liver has decreased during hypotensive anesthesia. Urine volume in the PGE1 group was larger than that in the TNG, SNP or LID group. CCR in the PGE1 group was larger than that in the NIC, TNG or SNP groups. CPAH in the PGE1 group was larger than that in the SNP or LID group. The value of urine NAG in the TNG group was larger than that in the NIC or PGE1 group. The value of urine beta 2-microglobulin in the NIC group was larger than that in the PGE1 or SNP group. The results of urine volume, CCR, CPAH, urine NAG, and urine beta 2-microglobulin indicate that blood flow to the kidneys was greater in the PGE1 group as compared to other groups. This study indicates that prostaglandin E1 is the best hypotensive drug for hepatic and renal blood flow during hypotensive anesthesia.
Aged↗
Mechanisms in acute oliguric renal failure induced by tetracycline infusion.
Tetracycline hydrochloride (TC), 30-70 mg/kg infused intravenously in dogs in the course of a few minutes, reduced clearance of inulin (Cin) and p-aminohippuric acid (CPAH) on an average to less than 5% of control. In spite of increased intrarenal pressure (approximately 50 mm Hg), electromagnetically recorded renal blood flow was preserved, indicating that the reduction of Cin and CPAH resulted from tubular obstruction, not renal vasoconstriction. The metabolic rate of the cortex and outer medulla fell to 69% of control after TC, as measured by the heat accumulation rate. Further reduction to basal metabolic level (30% of control) was reversibly produced by elevating ureteral pressure, suggesting that the high metabolic rate was caused by continued active reabsorption of sodium chloride at about half the control rate. Thus Cin greatly underestimated glomerular filtration rate in the TC-damaged kidney. From these results and the observation of TC-containing casts in the medullary tubules, we conclude that TC caused tubular obstruction and that leakage of inulin and PAH from the tubules occurred mainly distally to the major sodium-reabsorbing tubular segments.
Acute Kidney Injury↗
Renal handling of alendronate in rats. An uncharacterized renal transport system.
Alendronate (4-amino-1-hydroxybutylidene-1,1-bisphosphonate), an antiosteolytic agent, is currently under investigation in the treatment of a variety of bone diseases. Earlier studies from this laboratory have demonstrated that systemically administered alendronate is rapidly either taken up by bone tissues or excreted by the kidney, and that renal excretion is the only route of elimination. The purpose of this study is to characterize the renal handling of alendronate in rats by standard clearance procedures with inulin as a marker of glomerular filtration rate. Alendronate is highly bound to rat serum protein. The excretion of alendronate by the kidney is concentration-and dose-dependent, and saturable, indicating that it is secreted by an active transport mechanism. The secretory mechanism exhibits limitation of transport, with an apparent Tm of approximately 25 micrograms/min/kg. However, high doses of cimetidine, quinine, probenecid, and p-aminohippuric acid had no effect on the renal excretion of alendronate, suggesting that alendronate is not secreted by anionic or cationic transport systems. In contrast, alendronate clearance is inhibited by etidronate, another bisphosphonate, in a dose-dependent manner, implying that these two bisphosphonates compete for an as yet uncharacterized renal transport system. As expected, the renal excretion of alendronate is drastically reduced in rats with acute renal failure. As a consequence of renal impairment, alendronate accumulates in plasma, and the concentration of the drug in bone tissues increases significantly.
Alendronate↗
Long-term antihypertensive and renal effects of isradipine in hypertensive patients with normal and reduced renal function.
The long-term hemodynamic and antihypertensive effects of isradipine were investigated in 11 patients who had normal renal function and 9 who had reduced renal function. The dose regimen was 1.25-5 mg twice daily, depending on blood pressure response. After 24 weeks of active treatment, systolic/diastolic blood pressure decreased from 172/106 to 155/94 mm Hg (p less than 0.05) in the patients with normal renal function, and from 176/105 to 169/93 mm Hg (p less than 0.01) in those with impaired renal function. Contrary to the results of short-term treatment, no changes in inulin and p-aminohippuric acid (PAH) clearances were observed in either study group. There were no significant changes in plasma renin, aldosterone, glucose, or lipids, nor were these changes in protein excretion in either group; however, sodium excretion increased significantly in both groups. On the basis of our results, we conclude that isradipine has a place in the treatment of hypertensive patients with mild renal insufficiency.
Administration, Oral↗
Role of angiotensin II in the antinatriuresis that follows acute volume depletion.
The aim of this study was to examine the contribution of the renin angiotensin system to the antinatriuresis that follows acute volume depletion. Four groups of six dogs each were studied. The first group was exposed to saline expansion (8% body weight) (SE). The second group was exposed to acute volume depletion (2% body weight) followed in one hour by saline expansion (AVD). The third and fourth groups were similar but in dogs treated with high doses of captopril (SE + C and AVD + C). Dogs were anesthetized with phenobarbital. Control measurements were made for 30 minutes before and 60 minutes during saline expansion. Glomerular filtration rate (inulin), renal blood flow (para-aminohippuric acid) and mean arterial pressure were similar in the four groups during the experiment. The increase in fractional sodium excretion from the control period to the end of saline expansion was in the SE group from 0.6 +/- 0.2 to 6.4 +/- 1% and in the SE + C group from 1.1 +/- 0.3 to 8.5 +/- 1.3%. In contrast, in the AVD group it only rose from 0.8 +/- 0.2 to 3.5 +/- 0.7% and in the AVD + C group from 1.3 +/- 0.4 to 4.1 +/- 0.6%. Therefore, the increment in sodium excretion during saline expansion was significantly lower in dogs exposed to acute volume depletion, independent of the treatment with captopril. The blunted natriuresis cannot be explained by differences in GFR, RBF or MAP. These results suggest that renin angiotensin system is not the responsible agent of the sodium retention that follows acute volume depletion.
Acute Disease↗
Potential role of the renal tubule in fixing the level of plasma sulfoconjugated catecholamines in the dog.
Plasma levels of sulfoconjugated catecholamines in human subjects and in dogs are usually much higher than those of native amines. Their origins and the mechanism(s) involved in fixing their plasma concentrations are not well known; however, several lines of clinical evidences indicate a major role for the kidney. Thus this study was undertaken to measure the renal fractional excretion--used as an overall index of kidney mechanisms involved in the handling of catecholamines and their sulfoconjugates in the dog--and to look for any possible relationships between plasma concentration and urinary excretion. This was carried out in 36 anesthetized hydropenic mongrel dogs. The mean values of the renal fractional excretion of sulfoconjugated dopamine, norepinephrine, and epinephrine were shown to be statistically greater than 100%, suggesting a predominant secretion by the renal tubules of hydropenic dogs. Statistically significant correlations between plasma concentration and urinary excretion of sulfoconjugates--independent of blood pressure, cardiac output, clearance of para-aminohippuric acid, glomerular filtration rate, and sodium excretion are reported. Thus any change in the tubular handling of sulfoconjugates is likely to have a direct consequence in the fixation of their plasma concentrations.
Animals↗
Early morphological changes of tubules in rats with chronic renal failure.
We investigated the early changes of tubules and effect of the oral adsorbent, AST-120, on the early changes of tubules in rats with chronic renal failure. Sprague-Dawley rats were divided into two groups with and without AST-120, after 3/4 nephrectomy. Although there were no significant differences in levels of blood urea nitrogen, serum creatinine, creatinine clearance, inulin clearance, para-aminohippuric acid clearance and urinary N-acetyl-beta-D-glucosaminidase at week 8 between the two groups, the amount of 24-hour urinary protein excretion and the direct systolic blood pressure at week 8 were significantly decreased in the group with AST-120. Examinations by light microscopy at week 8 revealed that proteinaceous casts in the tubules, tubular dilatation and infiltration of monocytes into the interstitium in the group with AST-120 were less prominent than those in the group without AST-120. A significant difference in numbers of proteinaceous casts was noted at week 8 between the two groups. In rats with chronic renal failure at the early stage, it is concluded that the formation of proteinaceous casts, resulting in tubular damage, is increased and that AST-120 delays the occurrence of proteinaceous casts by delaying the increase in urinary protein excretion.
Adsorption↗
Transport of organic cations by a renal epithelial cell line (OK).
The goal of this study was to determine the mechanisms involved in the transport of the organic cation, tetraethylammonium (TEA), across the apical membrane of OK cells. [14C]TEA accumulated in OK cell monolayers reaching equilibrium in 2 h. The uptake of [14C]TEA at equilibrium was dependent upon temperature and was inhibited by sodium azide and by various organic cations, including N1-methylnicotinamide (NMN), mepiperphenidol, and cimetidine but not by the organic anion, p-aminohippuric acid. The initial uptake of [14C]TEA was characterized by a saturable process. The mean +/- S.D. Km was 27.8 +/- 2.6 microM and the Vmax was 414 +/- 26.5 pmol/mg protein/min. Both an accelerated efflux and influx of [14C]TEA in the presence of a trans-gradient of unlabeled TEA and NMN was observed, whereas a deaccelerated influx and efflux was observed in the presence of a trans-gradient of mepiperphenidol. The mechanism of interaction between NMN and TEA was examined. NMN significantly increased the apparent Km (mean +/- S.D.) of TEA to 82.8 +/- 16.4 microM (p less than 0.001), whereas the Vmax (mean +/- S.D.) was only slightly affected (478 +/- 72 pmol/mg protein/min) suggesting a competitive inhibition. The stimulatory effect of trans-gradients of NMN on TEA transport was due to an increase in the Vmax of TEA suggesting that NMN trans-stimulates TEA transport by increasing the turnover rate of the exchanger. In the presence of an inwardly directed proton gradient, the efflux at 30 s of [14C]TEA from the OK cell monolayers was significantly accelerated (p less than 0.05). Studies with the pH-sensitive fluorescent probe, 2',7'-bis(carboxyethyl)-5(6)-carboxyfluorescein, suggested that TEA could drive the countertransport of protons. In apical membrane vesicles prepared from OK cells, the uptake of [3H]NMN exhibited an apparent "overshoot phenomenon" in the presence of an initial outwardly directed proton gradient. Protons competitively inhibited TEA uptake suggesting that the proton/organic cation and the organic cation/organic cation self exchange mechanism are the same mechanism. This is the first report describing both TEA self-exchange and proton/TEA exchange in the apical membrane of a continuous cell line. OK cells are an excellent model for the study of organic cation transport across the apical membrane.
Animals↗
Glomerular hyperfiltration indicates early target organ damage in essential hypertension.
In 111 patients with essential hypertension (World Health Organization stage I or II), we examined the relationship between renal hemodynamics and left ventricular hypertrophy. Left ventricular structure was determined by two-dimensional guided M-mode echocardiography, renal blood flow by iodine I 131 aminohippuric acid clearance, and glomerular filtration rate by creatinine clearance. The glomerular filtration rate correlated with left ventricular mass (r = .52) and left ventricular cross-sectional area (r = .21). Conversely, at a similar age, body mass index, body surface area, and arterial pressure, hypertensive patients with left ventricular hypertrophy disclosed a higher glomerular filtration rate and filtration fraction than those without left ventricular hypertrophy, whereas renal blood flow and renal vascular resistance measurements were not significantly different. Thus, at similar levels of arterial pressure and renal blood flow, glomerular hyperfiltration was linked to early cardiac structural changes in essential hypertension. We conclude that, in a hypertensive patient with normal renal function, a high glomerular filtration rate may be an indicator for early target organ damage in essential hypertension.
Adult↗
The renal functions following a profound hypothermia in rats.
The aftereffects of renal function were studied in rats exposed to profound hypothermia and 5 min of cardiac arrest. All experimental rats were reanimated and survived at least 1 week. It was observed that the water intake and the basal renal excretion of urine, potassium and urea were decreased 24 hr after cooling, but did return to normal within 1 week. The renal handling of a large volume of infused saline was retarded 4 hr but recovered by the end of 24 hr after hypothermia. At both 4 and 24 hr after deep cooling, clearance of inulin and p-aminohippuric acid showed there were no change in glomerular filtration rate and effective renal plasma flow. It was concluded that the renal function was altered shortly after deep cooling and 5 min of cardiac arrest, however, this alteration could be completely recovered thereafter.
Animals↗
Species comparison of drug absorption from the lung after aerosol inhalation or intratracheal injection.
To compare the rates of pulmonary absorption of aerosolized and intratracheally injected drugs in the mouse, rabbit, and rat, anesthetized mice and rabbits prepared with a tracheal cannula inhaled a liquid aerosol or received an intratracheal injection of a drug solution by methods previously used in studies on the rat. Aerosols had mass median aerodynamic diameters in the range of 2.28-3.10 microm and geometric standard deviations in the range of 2.35-2.81. The volumes of solution injected intratracheally were approximately 2% of lung volume. At various times after drug administration, the lungs were removed and assayed for unabsorbed compound. Although the 12 drugs studied had widely different absorption rates, each was absorbed approximately 2 times more rapidly when inhaled as an aerosol than when administered by intratracheal injection, suggesting that absorption may be more rapid from the alveolar region than from the tracheobronchial region of the lung. With lipid-insoluble drugs, such as urea, benzylpenicillin, p-aminohippuric acid, mannitol, N-acetylprocainamide ethobromide, sucrose, and inulin, each was absorbed roughly 2.5 times faster in the mouse than in the rat, and roughly 2.5 times more slowly in the rabbit than in the rat. In contrast, with lipid-soluble drugs, such as antipyrine, salicylic acid, barbital, amitrole and procainamide, each was absorbed at about the same rate in all three species. The results suggest that the porosity of the pulmonary membrane is greatest in the mouse, lower in the rat, and lowest in the rabbit. The observed interspecies relationships in absorption rates suggest that it may be possible to predict the rate of absorption of a given drug in one species from data obtained for the same drug in another species.
Absorption↗
Effects of quinidine on the renal tubular and biliary transport of digoxin: in vivo and in vitro studies in the dog.
Quinidine is known to inhibit the renal clearance of digoxin without affecting glomerular filtration rate. The renal interaction between these drugs was investigated by a combination of in vivo and in vitro methods. The uptake of digoxin by brush border membrane vesicles was not affected by quinidine. Similarly, digoxin did not inhibit the uptake of the cation N-methylnicotinamide by these vesicles and did not alter the binding kinetics of digoxin to the Na+, K+-adenosine triphosphatase by the antiluminal membrane vesicles. By using the in vivo multiple indicator dilution technique transtubular transport of digoxin was documented; renal-artery infusion of quinidine did not affect the recovery of digoxin in the renal vein or urine. Clearance studies documented that the decrease in the renal clearance of digoxin is paralleled by a significant fall in renal blood flow evidenced by a decrease in p-aminohippuric acid clearance. It is concluded that quinidine inhibits the renal excretion of digoxin not by competition at the tubular cell membrane level, but rather by decreasing renal blood flow. A parallel decrease in biliary clearance of digoxin is documented and may suggest a similar mechanism.
Animals↗