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G Kuramochi

Publications and source records attributed to G Kuramochi.

16 recordsLinked to original sources
PubMed1997

Ochratoxin A disturbs pH homeostasis in the kidney: increases in pH and HCO3- in the tubules and vasa recta.

This study was designed to elucidate the effects of ochratoxin A (OTA) on pH homeostasis in the kidney. We measured pH in the proximal (PT) and the distal (DT) tubular fluid, the collecting duct urine (CD), the descending and the ascending vasa recta blood (VR), and the renal arterial blood (RA). OTA increased pH significantly in PT, DT, CD as well as in the descending and ascending VR, whereas pH in RA remained unchanged. We further determined CO2 tension (pCO2) and HCO3- in PT, CD as well as in the descending and ascending VR. OTA significantly increased HCO3- in PT, CD and the descending and ascending VR, with no changes in pCO2. Therefore, the increases in pH in PT, CD and the descending and ascending VR result from the increase in HCO3-. Our results suggest that OTA inhibits HCO3- reabsorption in the tubules, leading to the impairment of urinary acidification, and that OTA further leads to the disturbance of the acid-base state (alkalinization) in the interstitium in renal papilla. The impairment of urinary acidification may contribute to the disturbance of pH homeostasis in the renal papilla. The disturbance of pH homeostasis by OTA could be related to its nephrotoxicity.

Animals↗
PubMed1997

Derangement of pH homeostasis in the renal papilla: ochratoxin A increases pH in vasa recta blood.

It is reported that ochratoxin A (OTA) impairs urinary acidification by increasing the urinary pH and also increases the intracellular pH in Madin-Darby canine kidney cells. This study was designed to examine whether OTA deranges pH homeostasis in the interstitium (or vasa recta) of the renal papilla. Rats were injected once with OTA (3 micromol/kg body weight) intravenously (acute application) or with OTA (1.25 micromol/kg body weight/day) intraperitoneally for 6 days (subchronic application). We measured the pH values in both the descending and ascending vasa recta blood (VR) in the renal papilla. Both the acute and subchronic applications of OTA led to significant increases in pH values in both descending and ascending VR by 0.4-0.6 pH units. However, no significant increases in pH values in renal arterial and aortic blood in OTA-treated rats were observed. We also examined the pH changes in collecting-duct urine after OTA injection (3 micromol/kg body weight). We found a significant increase in pH values 30 min after OTA injection; this significant elevation of pH values was present during the whole experiment (120 min). The results of this study suggest that OTA deranges pH homeostasis in the interstitium of the renal papilla, in addition to the impairment of urinary acidification.

Animals↗
PubMed1996

Changes in the countercurrent system in the renal papilla: diuresis increases pH and HCO3- gradients between collecting duct and vasa recta.

This study was designed to elucidate the acid-base balance local to the collecting duct urine (CD) and vasa recta blood (VR) in the rat renal papilla in diuresis. The pH changes were measured in both a furosemide-induced and a volume-load-induced diuresis, whereas the PCO2 (i.e., CO2 tension) and HCO3- concentration were measured only in a furosemide-induced diuresis. In an antidiuresis, the pH of the VR was more acidic than that of the systemic arterial blood (DeltapH = 0.44-0.73). Additionally, the pH of the ascending VR was significantly lower than that of the descending VR (DeltapH = 0.14-0. 16). In diuresis, the pH of the CD decreased (DeltapH = 0.81-0.97), while the pH of the descending and the ascending VR increased; however, the increase was only significant in the ascending VR (DeltapH = 0.23-0.30). Consequently, the significant difference in the pH gradient between the descending and the ascending VR was eliminated. The PCO2 values in the CD and the ascending VR were not different from those in antidiuresis, while the HCO3- concentration in the CD and the ascending VR, respectively, decreased and increased significantly. Thus, in diuresis, the decrease in the pH of the CD and the increase in the pH of the ascending VR result, respectively, from the decrease and the increase in the HCO3- concentration, with no changes in the PCO2 values.

Animals↗
PubMed1994

Effects of D-glucose on oxygen consumption of renal cortex suffering from ischemic injury.

Alterations of Na(+)-dependent D-glucose transport in the proximal tubules resulting from ischemic injury were investigated. We measured the cortical oxygen (O2) consumption at various concentrations of exogenous D-glucose 1 day after ischemic injury in a kidney in which ischemia was induced by complete unilateral renal artery occlusion for 60 minutes and in a contralateral non-ischemic (control) kidney. Both kidneys exhibited a D-glucose concentration-dependent increase in O2 consumption. The increases in O2 consumption in both kidneys exhibited Michaelis-Menten-type saturation kinetics. However, increased Km and decreased Vmax were observed in the ischemic kidney. Phlorizin significantly inhibited O2 consumption in both kidneys at 5 mM, but the effect was not significantly at 0 mM of D-glucose. In contrast, ouabain significantly inhibited O2 consumption in both kidneys at 0 and 5 mM of D-glucose. The level of O2 consumption inhibition by phlorizin and ouabain in the ischemic kidney was markedly less than in the control kidney. The present study demonstrated that the decreased Na(+)-dependent D-glucose transport capacity can be attributed to a reduction in both phlorizin-sensitive transport capacity for D-glucose and ouabain-sensitive Na+, K(+)-ATPase activity 1 day after 60 minutes of ischemia.

Animals↗
PubMed1993

Effects of furosemide on renal oxygen consumption after ischemia in normal and streptozotocin diabetic rats.

Normal and streptozotocin diabetic rats were subjected to ischemic injury by unilateral renal artery occlusion for 60 min. The cortical and the medullary oxygen consumption (QO2) in the postischemic and the control, contralateral nonischemic, kidneys were measured 1 h, 1 day, and 1, 2 and 4 weeks for normal rats and 1 day, and 1 and 4 weeks for diabetic rats after ischemia. The effects of furosemide on QO2 of the cortex and the medulla of normal and diabetic rats were studied. The diabetic kidney was more vulnerable to ischemic injury than the normal kidney. Furosemide-sensitive active transport function in the medulla of the diabetic kidney was higher than that of the normal kidney. Furosemide did not decrease the cortical QO2 significantly in the control and the postischemic kidneys of normal and diabetic rats. In contrast, the medullary QO2 of the control kidney in both rats was significantly reduced by furosemide at every period after ischemia. In the medullary QO2 of the postischemic kidney, there were no significant decreases at any period after ischemia in the diabetic rats and only after a 1-hour period for normal rats. However, 4 weeks after ischemia, there was no statistically significant difference in the medullary QO2 inhibition by furosemide between the control and the postischemic kidneys in both normal and diabetic rats. We conclude that the furosemide-sensitive active transport function in the medulla recovers by the 4th week after ischemia in normal and diabetic rats.

Animals↗
PubMed1993

Postischemic recovery process of renal oxygen consumption in normal and streptozotocin diabetic rats.

We tried to study in depth the recovery process in the cortical and the medullary oxygen (O2) consumption of normal and streptozotocin diabetic rat kidneys after ischemia. It was found that the cortical and the medullary O2 consumption decreased after ischemia, reaching their lowest levels at 1 day after every ischemic duration in normal and diabetic kidneys. In the period prior to ischemia to 1 day after ischemia, no significant difference was seen in the decrease in O2 consumption between the cortex and the medulla in normal kidney, whereas the medullary O2 consumption significantly decreased compared with the cortical O2 consumption in diabetic kidney. From 1 day to 4 weeks after ischemia, the increase in the cortical O2 consumption was significantly higher than that in the medulla of normal kidney. In contrast, the increase in the medullary O2 consumption was significantly higher than that in the cortex of diabetic kidney. Consequently, up to 4 weeks after ischemia, the decrease in the cortical O2 consumption was significantly lower than in the medulla of normal kidney, while there was no significant difference regarding the decrease in O2 consumption between the cortex and the medulla in diabetic kidney. These results suggest that there is a clear difference in the postischemic recovery process of O2 consumption between the cortex and the medulla, and also between normal and diabetic rat kidneys.

Animals↗
PubMed1993

Effects of theophylline, verapamil, and mannitol on oxygen consumption of ischemic rat kidneys.

This study was designed to determine, through the measurement of oxygen consumption (QO2), whether pretreatment and posttreatment with theophylline, verapamil, and mannitol provide protection from damage in the cortex and medulla of rat kidneys subjected to 60 and 120 minutes of ischemia. QO2 levels in both tissues were examined 1 day after each ischemia. After 60 minutes of ischemia, pretreatment with theophylline and verapamil primarily provided protection from ischemic change in cortical QO2. Pretreatment with mannitol provided protection from both cortical and medullary changes in QO2, but posttreatment with mannitol only protected cortical QO2. After 120 minutes of ischemia, only pretreatment with verapamil was effective in protecting cortical QO2 from ischemic injury. These observations demonstrate that theophylline, verapamil, and mannitol are effective in protecting renal QO2 in the ischemic kidney. During this study, it became clear that there were differences in the effectiveness of theophylline and verapamil on QO2 in the ischemic kidney between pretreatment and posttreatment, and also between the cortex and the medulla.

Animals↗
PubMed1989

[Efficacy and safety of long-term and low-dose desferrioxamine therapy against hyperaluminemia and the clinical symptoms associated with hyperaluminemia in patients undergoing maintenance hemodialysis].

In order to examine the efficacy and safety of long-term and low-dose desferrioxamine (DFO) therapy against hyperaluminemia and the clinical symptoms associated with hyperaluminemia, 4 patients (3 men and 1 woman, 40-62 years old, period of hemodialysis: 69-189 months) undergoing maintenance hemodialysis were treated by DFO (0.5 g/week) and hemodiafiltration for 27 weeks. 1 patient had only hyperaluminemia, but other 3 patients had refractory ostalgia and arthralgia associated with hyperaluminemia. Clinically, ostalgia and arthralgia disappeared within 1 month after the initiation of treatment. The decrease of serum aluminum level was recognized in all patients (74 +/- 7 micrograms/l to 52 +/- 7 micrograms/l). Also the decrease of delta aluminium was recognized in 2 patients. Serum iron levels did not change, but unsaturable iron binding capacity levels increased slightly. Serum ferritin level decreased in 1 patient. Serum PTH-C levels increased slightly in 3 patients. Serum total protein and albumin levels did not change. Serum transferrin levels increased slightly. Bone mineral contents were measured by microdensitometry method. In 1 patient with only hyperaluminemia, MCI and S.GS/D ameliorated remarkably. Side effects were not recognized in all patients during the course of treatment with DFO. In conclusion, it was thought that the treatment of long-term and low-dose DFO was effective and safe against hyperaluminemia and aluminium intoxication in patients undergoing maintenance hemodialysis.

Adult↗
PubMed1986

Dependence of oxygen consumption on Cl- transport and metabolic substrates in the early distal tubule of the Triturus kidney.

The early distal tubule (eDT) and the proximal tubule (PT) were dissected as tissue samples from the Triturus kidney. The oxygen consumption (QO2) of these tubules was measured and the effects on QO2 by transport inhibitors and metabolic substrates were studied. In eDT, complete Cl- replacement with NO3- or an addition of furosemide (2 X 10(-5) M) reduced Qo2 from 8.4 +/- 1.7 to 4.4 +/- 0.8 or from 8.3 +/- 1.6 to 4.4 +/- 0.6 nl X min-1 X mg-1 (dry weight), respectively. Also Na+ replacement with choline or with an addition to ouabain (1 X 10(-3) M) reduced QO2 from 5.9 +/- 0.8 to 3.4 +/- 0.4 or from 13.2 +/- 1.8 to 4.7 +/- 0.3 nl X min-1 X mg-1 (dry weight), respectively. In PT, complete Cl- replacement with NO3- or the addition of furosemide did not affect QO2 significantly, but Na+ replacement with choline or the addition of ouabain reduced it from 8.1 +/- 1.0 to 5.4 +/- 0.7 or from 10.8 +/- 0.9 to 7.4 +/- 0.8 nl X min-1 X mg-1 (dry weight), respectively. The data indicate that about a half of the QO2 in eDT is linked to active Cl- transport, in PT, Cl- is not transported actively and is not affected by furosemide. Effects on QO2 by various metabolic substrates, including TCA-cycle intermediates and metabolizable amino acids and carboxylic acids were tested. Among them, succinate, L-glutamate, L-aspartate, citrate, and acetate were found to effectively increase the QO2. The substrate-dependencies of QO2 in eDT were very similar to those in PT, in kinds of effective substrates and in the extent of increase. These findings suggest that, in eDT and PT, the uptake mechanisms for substrates and their coupling with aerobic metabolism are very similar.

Amino Acids↗
PubMed1986

Effect of D-glucose on oxygen consumption of renal proximal tubules of the Triturus.

Effect of exogenous D-glucose on oxygen consumption (QO2) was investigated in the proximal tubules of the Triturus kidney. In the proximal tubule, which was perfused and incubated with a solution containing Na+, QO2 was increased dependently of the concentration of added glucose. By removal of Na+ from the perfusate and incubation solutions, QO2 kept the level even by increasing adding glucose. The glucose dependence of Qo2 in the proximal tubule showed the saturable manner of a Michaelis-Menten type and gave a half saturation concentration of 1.3 mM. When phlorizin (1 X 10(-3) M) or ouabain (1 X 10(-3) M) was added to the perfusate and incubation solutions, the glucose dependency of QO2 was abolished, even in the Na+-containing solution. When alpha-methyl-D-glucoside (alpha-MG) was used instead of D-glucose, the QO2 of the proximal tubule showed a dependency on the concentration of alpha-MG. On the other hand, when D-mannitol was used instead of D-glucose, the QO2 was independent on the concentration of D-mannitol. The increase in QO2 of the proximal tubule by exogenous D-glucose could be explained by the stimulation of the Na+ pump, which is the consequence of enhanced Na+ entry through Na+/D-glucose cotransport across the luminal membrane.

Animals↗
PubMed1983

Lumen-positive chloride transport potential in the early distal tubule of Triturus kidney: its absolute dependence on the presence of Na+ and K+ in the luminal fluid.

Microperfusion experiments with Na+-free and/or K+-free solutions revealed that the generation of Cl- -dependent lumen-positive transtubular potentials of the early distal tubule of Triturus kidney was absolutely dependent on the presence of both Na+ and K+ in the lumen. Increases in luminal Na+ or K+ concentration increased the luminal positivity in a saturable manner, and the half saturation concentration was found to be about 1 mM for both cations. The results strongly suggest that Cl- is cotransported with Na+ and K+ across the luminal membrane.

Animals↗
PubMedDate not supplied

Regulation of the urine concentration mechanism by the oropharyngeal afferent pathway in man.

BACKGROUND: It has been reported that the oropharyngeal afferent pathway behaves as a first-order factor regulating body fluid. However, the neural mechanism has not yet been clear. This study was designed to elucidate the characteristics of the neural mechanism in man. METHODS: Healthy human subjects kept either an isotonic or hypertonic solution in the oral cavity so as to moisten the oropharyngeal mucosa without intake for 20 min. Plasma vasopressin (AVP) concentration, urine volume and urine and plasma osmolalities were measured before and after the application. RESULTS: The oropharyngeal application of isotonic saline induced no significant changes in plasma AVP concentration, urine volume and osmolality, while that of hypertonic saline induced a significant decrease and increase in urine volume and osmolality, respectively. The plasma AVP concentration increased significantly after the application of hypertonic saline. Mannitol also induced a significant decrease and increase in urine volume and osmolality, respectively. However, the urinary responses after the application of mannitol were delayed compared with those of hypertonic saline. There were no significant changes in plasma osmolality before and after each application. CONCLUSION: These results suggest that the oropharyngeal afferent pathway from the oropharynx to hypothalamic AVP-producing cells takes part in the thirst mechanism regulating body fluid in humans. The oropharyngeal afferent signals may behave as sodium-chloride-sensitive osmoreceptor.

Adult↗