Renal concentrating defect and organic osmolytes. Paradoxical changes of renal medullary taurine contents in potassium-depleted rats.
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Animals↗
Biomedical subjects
Y Takamitsu
Publications and source records attributed to Y Takamitsu.
Na+/myo-inositol cotransport is regulated by tonicity in cultured rat mesangial cells.
Mesangial cells are considered to be faced with osmotic stress under physiological (such as extraglomerular mesangial cells) and pathophysiological (for example, diabetes mellitus) conditions. To see if mesangial cells have an osmoregulatory mechanism, like renal medullary cells, we measured the intracellular contents of organic osmolytes in isotonic and hypertonic conditions. Cultured rat mesangial cells are well tolerant of acute increase in osmolality up to 500 mOsm/kg. The myo-inositol content increased in hypertonic cells more than six-fold the value in isotonic cells. The contents of glycerophosphorylcholine and sorbitol also increased but were less than that of myo-inositol. The Na(+)-dependent myo-inositol uptake in hypertonic cells was a 12-fold uptake in isotonic cells, reaching a maximum 24 hours after the switch to a hypertonic medium. The uptake rate increased as medium osmolality increased from 300 to 500 mOsm/kg. Raffinose is the most effective solute to increase the myo-inositol uptake. NaCl, glucose and mannitol also increased the uptake rate (NaCl > glucose > mannitol). The increased uptake by hypertonicity was the result of an increase in Vmax without change in Km and was dependent on RNA and protein synthesis. These results indicate that mesangial cells respond to extracellular hypertonicity by increasing myo-inositol transport activity and accumulating myo-inositol into the cells, suggesting that myo-inositol functions as an organic osmolyte in mesangial cells.
Animals↗
Elevated serum pepsinogens in chronic renal failure patients.
Human pepsinogens, the precursors of pepsin, originating from the stomach mucosa, are classified into two biochemically distinct groups, namely pepsinogen I (PG I) and pepsinogen II (PG II). We studied the serum levels of PG I and II in 51 normal volunteers, 23 chronic glomerulonephritis patients, 21 continuous ambulatory peritoneal dialysis (CAPD) patients and 40 hemodialysis patients. Serum pepsinogen levels were measured with a competitive binding double antibody radioimmunoassay. In the group of chronic glomerulonephritis patients, a positive correlation between the serum creatinine and the pepsinogen levels were found. The serum pepsinogen levels were remarkably elevated in CAPD and hemodialysis patients. The median levels of post-hemodialysis PG I (265.4 +/- 165.2 ng/ml) and PG II (41.7 +/- 38.0 ng/ml) were significantly higher than prehemodialysis values (PG I 207.4 +/- 127.5 ng/ml, PG II 29.0 +/- 16.6 ng/ml). Pepsinogen release by isolated gastric glands of guinea pigs was suppressed by guanidinosuccinic acid and was facilitated by calcium. The data suggest that both removal of guanidinosuccinic acid and infusion of calcium during hemodialysis contribute to the raised serum levels of these pepsinogens after hemodialysis.
Adult↗
Effect of 1,25-dihydroxyvitamin D3 and diltiazem on tissue calcium in uremic rat.
The concentration of calcium was measured in the aorta, heart, and kidney of uremic rats treated with 100 ng/kg/day 1,25-dihydroxyvitamin D3 (1,25 D3) or 60 mg/kg/day diltiazem for 12 weeks. The concentration of calcium was increased in the aorta, heart, and kidney of uremic rats, and was further increased by administration of 1,25 D3. The 1,25 D3-induced increase in calcium in the aorta was inhibited by diltiazem, but this effect was not accompanied by a decrease in serum calcium x phosphate products. Diltiazem had no effect on the 1,25 D3-induced increase of calcium in the heart and kidney. Thus, in uremia 1,25 D3 may promote the calcification of the aorta; calcium antagonists may protect against calcification without a reduction in serum calcium x phosphate products.
Animals↗
[Chylomicron and VLDL metabolism in daunomycin-induced nephrotic rats].
Lipid metabolism in chylomicron and VLDL were examined in daunomycin-induced nephrotic rats. 1) There was no difference in intestinal cholesterogenesis between the control rats and daunomycin-induced nephrotic rats. 2) The apoprotein content of chylomicron and VLDL increased in daunomycin-induced nephrotic rats. 3) Daunomycin-induced nephrotic rats showed increases in the content of apo B-48 and C-III, and a decrease in that of apo E in chylomicron. The apoprotein composition of VLDL in daunomycin-induced nephrotic rats showed increased apo B and decreased apo E. These results suggest that increased chylomicron-cholesterol is not due to increased intestinal cholesterogenesis, but to decreased chylomicron catabolism in daunomycin-induced nephrotic rats. Increased apoprotein in VLDL may contribute to the decreased catabolism by reducing LPL activity in the plasma and increased secretion from the liver of daunomycin induced nephrotic rats.
Animals↗
[Perioperative management of dialysed patients for orthopedic surgery].
Recently, renal osteodystrophy is a remarkable problem in patients on long-term hemodialysis (HD). In this retrospective study, we evaluated the perioperative management of 21 patients receiving orthopedic surgery between January 1990 and December 1992. These patients had been maintained on HD for an average of 8.6 years (range, 18 months-20 years). The primary causes of orthopedic surgery were amyloidosis, diabetic gangrene, rheumatoid arthritis and fractures. Laminectomy, replacement of arthropathy, osteosynthesis and amputation of the lower extremity were undertaken. General anesthesia was performed on six patients. Vecuronium was given to all of these patients. Isoflurane was used in 5 patients and sevoflurane in 1 patient. Regional anesthesia was used in 15 patients. During anesthesia, the average infusion rate of intravenous fluids was 2.7 ml.kg-1.h-1, and the intraoperative complications included hypertension in 16, hypotension in 12, arrhythmia in 4 and prolonged sedation in 2 patients. Postoperative complications included hyperkalemia in 2, pneumonia in 2, psychological disorder in 3, clotting fistula in 1 and delayed wound healing in 7 patients. One early death in a diabetic patient following amputation occurred on the 13th postoperative day. Preoperative HD was performed within 24 hours and postoperative HD within 72 hours of the operation. Nafamostat mesilate was used as an anticoagulant. Excessive removal of potassium must be avoided during preoperative HD to prevent arrhythmia. The well-managed elective patients gave a good result. However, extreme care in nutrition and infection control should be taken, especially in diabetic patients.
Anesthesia↗
Role of taurine in the kidney: osmoregulatory taurine accumulation in renal medulla.
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Animals↗
Adsorption of human recombinant erythropoietin on dialysis membranes in vitro.
The adsorptive characteristics of 5 dialysis membranes for recombinant human erythropoietin (EPO) were studied in vitro in a closed circuit system. For 120 min, EPO added with bovine serum was significantly adsorbed by polymethylmethacrylate (PMMA) and polyacrylonitrile (PAN) membranes but not by Cuprophan, ethylene vinyl alcohol (EVAL), or polysulfone (PS) membranes. In addition the EPO adsorptive rate, as well as that of beta 2-microglobulin (beta 2-MG), was greater with a PMMA membrane than with a PAN membrane. EPO was not detected in the ultrafiltrate at 15 min with 5 membranes. These results indicate that EPO was eliminated by membrane adsorption only with some dialysis membranes.
Acrylic Resins↗
Impairment of renal medullary osmolyte accumulation in potassium-depleted rats.
To determine the relationship between accumulation of osmolytes and maximal urinary concentration in potassium depletion, we tested the effects of experimental water diuresis or potassium depletion on osmolytes in the renal medulla of rats. Hyperosmotic stress was imposed by 4 days of water deprivation for the purpose of establishing the maximal concentrating ability or by the infusion of sodium for the purpose of loading the equal amounts of sodium to the renal medulla. In the diuresis group, water deprivation failed to increase betaine, sorbitol, and taurine contents to the same level as the untreated group, although sodium infusion increased betaine and sorbitol. In the potassium depletion group followed by water deprivation, urine osmolality (2,490 +/- 241 vs. 3,425 +/- 268 mosmol/kgH2O) and all osmolytes were significantly lower than in the untreated group. In response to hyperosmolality with sodium infusion, myo-inositol and glycerophosphorylcholine contents rose to the level of the untreated group. Medullary betaine (67.6 +/- 6.8 vs. 99.5 +/- 8.9), taurine (44.7 +/- 2.4 vs. 61.4 +/- 6.2) and sorbitol (35.6 +/- 4.4 vs. 57.0 +/- 8.4 mmol/kg protein) contents were reduced in potassium-depleted rats when the renal medulla was as hypertonic as in the untreated group. In conclusion, the processing of betaine, taurine, and sorbitol accumulation appeared to be impaired in potassium depletion.
Animals↗
Organic osmolytes in rat renal inner medulla are modulated by vasopressin V1 and/or V2 antagonists.
For the purpose of clarifying the role of vasopressin V1 and V2 receptors in osmolyte accumulation, we determined the effects on the inner medullary osmolyte content of the administration of orally active vasopressin V1 and/or V2 receptor antagonists OPC-21268 (i.e., 1-(1-[4-(3-acetylaminopropoxy)benzoyl]-4-piperidyl)- 3,4-dihydro-2(1H)-quinolinone) and OPC-31260 (i.e., 5-dimethylamino-1-[4-(2-methylbenzoylamino)benzoyl]-2,3,4,5-tet rah ydro-1H- benzazepine] under a condition of maximal urine concentration achieved by water deprivation for 4 days. Taurine content increased significantly with the use of the V2 antagonist, irrespective of the use of the V1 antagonist. Inner medullary betaine content decreased with the administration of the V1 antagonist, irrespective of the administration of V2 antagonist. The administration of either the V1 or V2 antagonist alone did not affect sorbitol content, aldose reductase activity, or aldose reductase mRNA abundance in renal inner medulla. However, the combined administration of the V1 and V2 antagonists decreased all of these significantly. Myo-inositol content was not affected by the administration of the V1 or V2 antagonists. Glycerophosphorylcholine content was decreased with the use of the V2 antagonist, irrespective of the use of the V1 antagonist, and this effect paralleled urine osmolality. In conclusion, the individual organic osmolytes responded differently to the antagonists of vasopressin V1 and/or V2 receptors. The mechanisms linked to vasopressin V1 and/or V2 receptors appeared to modulate the accumulation of some organic osmolytes in the inner medulla. Aldose reductase mRNA abundance and sorbitol accumulation in the inner medulla appeared to be mediated through either V1 or V2 receptors.(ABSTRACT TRUNCATED AT 250 WORDS)
Aldehyde Reductase↗
In vivo osmoregulation of Na/myo-inositol cotransporter mRNA in rat kidney medulla.
myo-Inositol, a major compatible osmolyte in renal medulla, is accumulated in kidney-derived epithelial cells cultured in hypertonic media via Na/myoinositol cotransporter (SMIT). The altered medium osmolality of Madin-Darby canine kidney cells leads to changes in the transcription of the SMIT gene and mRNA abundance. To investigate whether SMIT is regulated by tonicity in vivo, renal medullary myoinositol and SMIT mRNA was measured in rats in hydrated and dehydrated states. Rats were divided into two groups: (1) hydrated rats, free access to 3% sucrose water; (2) dehydrated rats, 3 days of water deprivation. Urine sodium, potassium, urea, and osmolality in dehydrated rats were significantly higher than in hydrated rats. Renal medullary sodium, urea, and myo-inositol in dehydrated rats were significantly higher than in hydrated rats. Northern analysis revealed that there was a message hybridized to SMIT cDNA in the cortex and outer and inner medulla of the kidney. Compared with hydrated rats, SMIT mRNA in dehydrated rats was 2.6-fold higher in the outer medulla and 2.5-fold higher in the inner medulla. These results indicate that there is osmoregulatory SMIT in the outer and inner medulla of the kidney and that myo-inositol accumulation in this region is probably due to the increased expression of the SMIT gene.
Animals↗
Determinants of relative amounts of medullary organic osmolytes: effects of NaCl and urea differ.
Sorbitol, inositol, betaine, taurine, and glycerophosphorylcholine (GPC) are organic osmolytes that accumulate in the renal inner medulla during antidiuresis. In the cultured cell model, high medium sodium increases all the cell osmolytes and high medium urea increases cell GPC and inositol. It has been difficult, however, to discriminate between the effects of sodium and urea on organic osmolytes in water-deprived animals. To determine the nature of the in vivo responses of osmolyte accumulation induced by extracellular sodium or urea, we measured the medullary organic osmolytes and tested the degree of their linear correlation with urine and tissue parameters in control, dehydrated, salt-loaded, and urea-loaded rats. All of the osmolytes except myo-inositol increased in salt-loaded rats. Betaine and sorbitol contents in dehydrated rats were less than in salt-loaded rats, but other osmolytes increased significantly. Conversely, in urea-loaded rats, only GPC increased significantly, whereas either no change occurred for other osmolytes or sometimes betaine and sorbitol levels decreased. These data suggest that high sodium increases all of the osmolytes except myoinositol, whereas high urea increases only GPC and may decrease the renal medullary contents of betaine and sorbitol. We also demonstrated, using linear regression analysis, that urea and electrolyte in urine as well as tissue correlate well with each osmolyte measured.
Animals↗
Doppler sonographic measurement of phasic renal artery blood flow velocity in patients with chronic glomerulonephritis.
The phasic arterial blood flow velocity at the renal hilus was measured by Doppler sonography in 25 healthy subjects and 78 patients with chronic glomerulonephritis. Doppler velocity waveform was analyzed to give peak systolic velocity (S), end-diastolic velocity (D), resistive index (RI), and pulsatility index (PI). Creatinine clearance correlated with S (r = 0.76), D (r = 0.80), RI (r = -0.74), and PI (r = -0.85). Color Doppler sonography facilitated the detection of blood flow and permitted the measurement of absolute blood flow velocity, which previously had been difficult to determine. These results suggest that renal arterial blood flow as detected by Doppler ultrasonography may be useful for noninvasive, direct, rapid, and simple evaluation of renal function, although various modifying factors also need to be considered.
Adult↗
[Lipid metabolism in daunomycin-induced nephrotic rats (Part 6)].
Lipid metabolism in tissues and HDL were examined in daunomycin-induced nephrotic rats. 1) Daunomycin-induced nephrotic rats showed the decreased phospholipids, the increased cholesterol content in heart. Phospholipids, triglycerides and cholesterol content in brain, lung and spleen were similar in daunomycin-induced nephrotic rats and control rats. 2) Triglycerides content in hepatocytes was decreased in daunomycin-induced nephrotic rats. But, cholesterol esters content in hepatocytes was higher in daunomycin-induced nephrotic rats than control rats. 3) LCAT activity in serum was increased in daunomycin-induced nephrotic rats. 4) Apolipoproteins composition of HDL in daunomycin-induced nephrotic rats showed the increased apoA-I and the decreased apo E. These results show that the increased cholesterol esters in liver tissue are due to hepatocytes in daunomycin-induced nephrotic rats. The increased HDL cholesterol content may contribute to the increase of LCAT activity in daunomycin-induced nephrotic rats. The increase of LCAT activity in serum results in the increased apo A-I content in daunomycin-induced nephrotic rats. No direct evidence about the incorporation of HDL into liver is obtained from the present experiments and further study will be necessary to clarify this evidence.
Animals↗
Adsorption of nafamostat mesilate by hemodialysis membranes.
The adsorption of the anticoagulant nafamostat mesilate (FUT-175) by five different hemodialysis membranes was studied in vivo and in vitro. In vivo, FUT-175 was adsorbed strongly by a polyacrylonitrile (AN69) membrane and slightly by another polyacrylonitrile (J-PAN) membrane but not by Cuprophan (CU), hemophan (HE), or polymethylmethacrylate (PMMA) membranes during hemodialysis performed in 4 patients in whom FUT-175 was used as an anticoagulant. Only during hemodialysis using the AN69 membrane did FUT-175 not induce a significant prolongation of celite-activated coagulation time. In vitro studies showed that FUT-175 was adsorbed by the AN69, J-PAN, and PMMA membranes but not by the CU and HE membranes. Methylene blue, a dye that possesses a cationic portion in its chemical structure, stained AN69, J-PAN, and PMMA membranes. Since FUT-175 also possesses a cationic portion, we conclude that FUT-175 is adsorbed by negatively charged membranes via an ionic bond and is unsuited for use as an anticoagulant in hemodialysis using an AN69 membrane because of that membrane's marked capacity to adsorb FUT-175.
Adsorption↗
Dopaminergic modulation of the pressure-natriuresis response in rats.
OBJECTIVE: The present study was carried out to examine the involvement of dopamine in the pressure-natriuresis phenomenon which has been postulated as a major regulator of extracellular fluid volume and thereby arterial pressure. DESIGN: Dopaminergic modulation of the pressure-natriuresis response was studied in the innervated and denervated rat kidney, to allow a distinction between the effects of neural and extraneural dopamine. METHODS: The pressure-natriuresis response was studied in anesthetized Sprague-Dawley rats, in which neural and hormonal influences on the kidney were fixed by denervating the kidney and by intravenous infusion of aldosterone, hydrocortisone, vasopressin and norepinephrine. The innervation to the kidney remained intact in some experiments with the selective dopamine-1 antagonist SCH 23390. Urinary excretion of dopamine during the pressure-natriuresis response was also examined in the innervated and denervated rat kidney. RESULTS: Although infusion of dopamine at a dose of 2 micrograms/kg per min had no effect on the pressure-natriuresis response in rats in which neural and hormonal influences on the kidney were fixed, the slopes of the relations between urine flow, sodium excretion and mean arterial pressure in rats given 10 micrograms/kg per min dopamine were significantly greater than those found in the control rats. Renal plasma flow increased significantly in the dopamine-treated rats whilst glomerular filtration rate did not differ between the control and dopamine-treated rats. The dopamine-induced increase in the slope of pressure-natriuresis relationship and renal plasma flow were completely blocked by 0.5 micrograms/kg per min SCH 23390. However, infusion of SCH 23390 alone at 0.5 micrograms/kg per min did not significantly alter the pressure-natriuresis response in rats with either denervated or innervated kidney. In addition, urinary excretion of dopamine derived from neither neural nor extraneural origins was altered in parallel with variations in mean arterial pressure. CONCLUSION: These results suggest that exogenous administration of dopamine may affect the pressure-natriuresis response by altering the magnitude of arterial pressure-induced changes in tubular sodium reabsorption, via an action of dopamine-1 receptors. However, endogenous dopamine does not appear to be capable of modulating the pressure-natriuresis response.
Animals↗
[Doppler ultrasound measurement of phasic renal arterial blood flow velocity in patients with chronic glomerulonephritis].
The phasic renal arterial blood flow velocity was measured using a Doppler-Based Toshiba SSH-160A scanner in 25 healthy subjects and 78 patients with chronic glomerulonephritis. Renal arterial blood flow at the renal hilum was visualized with color Doppler ultrasound, and the velocity waveform was obtained by pulsed Doppler ultrasound. The velocity waveform was then analyzed to give the peak systolic velocity (S), end-diastolic velocity (D), resistive index (RI), and pulsatility index (PI). Creatinine clearance correlated with S (r = 0.76), D (r = 0.80), RI (r = -0.74), and PI (r = -0.85). The split renal glomerular filtration rate, calculated by a method which makes use of the early renal uptake of Tc-99m DTPA, also correlated well with these parameters. These findings suggest that renal arterial blood flow as detected by Doppler ultrasound may be useful for the noninvasive, direct, rapid, and simple evaluation of renal hemodynamics and renal function, although various modifying factors also need to be considered.
Adolescent↗
Noninvasive detection and monitoring of renal arteriovenous fistula by color Doppler.
The diagnosis of a renal arteriovenous fistula is usually confirmed by angiography. Described is the utilization of color Doppler ultrasound to monitor a renal arteriovenous fistula before and after treatment by transcatheter steel coil embolization in a 63-year-old woman. Using color Doppler, the arteriovenous fistula with an aneurysmal lesion was clearly visualized. A pulsed-wave Doppler analysis showed increased flow velocity and decreased pulsatility in the supplying artery. After successful transcatheter occlusion of the fistula, these findings disappeared. The Doppler ultrasound technique is likely to be useful to detect and monitor a renal arteriovenous fistula noninvasively, simply, and quickly.
Arteriovenous Fistula↗