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H Endou

Publications and source records attributed to H Endou.

At least 145 records · Page 8Linked to original sources
PubMed1986

Intra- and inter-nephron heterogeneity of gluconeogenesis in the rat: effects of chronic metabolic acidosis and potassium depletion.

The intra- and inter-nephron heterogeneity of renal gluconeogenesis within rat proximal tubules and the effects of chronic metabolic acidosis and chronic potassium(K)-depletion were studied using isolated proximal tubules of rats by directly measuring glucose synthesized. The gluconeogenic activity from pyruvate and glutamine in control rats was almost limited to within the early proximal tubule (S1: 45.4 +/- 5.7 pmol/mm/60 min from pyruvate; 58.0 +/- 6.0 from glutamine). Very low, but detectable gluconeogenesis was observed in the middle portion of the proximal tubule (S2: 9.9 +/- 2.2 from pyruvate; 4.8 +/- 1.1 from glutamine). The rate of glucose production in the terminal proximal tubule (S3) was negligible. Furthermore, gluconeogenesis from glutamine of superficial (SF) nephrons was significantly higher than that of juxtamedullary (JM) ones, whereas no difference was seen in gluconeogenesis from pyruvate. In acidotic and K-depleted rats, significant increase could be seen in S1 and S2, but the increase in S3 was not significant. By the serial determination in acidosis, the glucose production from both substrates was found to be the highest at the second 1 mm segment from the glomerulus, and it decreased downward along the proximal tubule. In acidosis, glucose production from both substrates in SF nephrons and that from glutamine in JM ones were elevated significantly compared with the control, but that from pyruvate in JM nephrons did not change. These results suggest that S1 of the SF nephron plays the most important role in gluconeogenesis in the control, whereas S1 of the JM nephron and S2 contribute to gluconeogenesis in acidotic and/or possibly K-depleted rats.

Acidosis↗
PubMed1986

Intra- and inter-nephron heterogeneity of ammoniagenesis in rats: effects of chronic metabolic acidosis and potassium depletion.

In order to determine intra- and inter-nephron heterogeneity of ammoniagenesis, ammoniagenic activity in microdissected nephron segments of control, acidotic and potassium (K)-depleted rats was examined. Intranephron distribution of ammoniagenic activity in control rats revealed the highest amount at the second segment of the proximal tubule (S2). Chronic metabolic acidosis induced ammoniagenesis markedly at the first segment of the proximal tubule (S1) by 235% and the thick ascending limb of Henle's loop by 198% and moderately at the S2 by 49%. K-depletion increased ammonia production significantly in the S1 by 298% and the S2 by 107%, which is a pattern quite similar to the result of chronic metabolic acidosis. Ammonia production in K-depletion was also increased in the cortical and medullary collecting tubule by 71% and 102%, respectively, probably due to increases in protein amounts (41% and 158%, respectively) there. To evaluate inter-nephron heterogeneity of ammoniagenesis, ammonia formation from glutamine in the S1 of superficial (SF) and juxtamedullary (JM) nephrons was examined. Although there was no difference in ammonia production between SF-S1 and JM-S1 in control rats, ammonia production in SF-S1 was significantly higher than that in JM-S1 in both metabolic acidosis and K-depletion. From these studies, we conclude: The increase of ammonia production in the proximal tubule was quite similar in both acidosis and K-depletion, suggesting that the main trigger of ammoniagenesis in both conditions might be a reduction of intracellular pH. SF-S1 was the nephron most reactive to acidosis and K-depletion. JM nephrons could be considered to be important not for ammonia production but for ammonia secretion.

Acidosis↗
PubMed1986

Evidence that alpha-1-adrenergic stimuli specifically increase gluconeogenesis of the isolated proximal convoluted tubule in the rat.

Isolated kidney-cortical tubule suspensions and microdissected nephron segments from fed rats were used to study the action of catecholamines on gluconeogenesis. Gluconeogenesis from rat tubule suspension incubated with 5 mM pyruvate was stimulated maximally by 10(-5) M methoxamine, an alpha 1-selective agonist, and 10(-6) M noradrenaline by 29.2 +/- 5.2% (mean +/- SEM) and 32.6 +/- 2.9%, respectively. These effects were completely inhibited by 10(-7) M prazosin, a beta 1-selective antagonist. Yohimbine, an alpha 2-antagonist, also inhibited the effect, but only at a higher concentration (5 X 10(-5) M). Gluconeogenesis was not stimulated by isoproterenol, a alpha-agonist, at any concentrations between 10(-5) and 10(-7) M. With microdissected nephron segments, only the proximal tubule possessed gluconeogenic activity. Within the proximal tubule, the proximal convoluted tubule (PCT) revealed higher gluconeogenic activity than the proximal straight tubule (PST). Methoxamine at 10(-5) M stimulated gluconeogenesis in PCT, whereas in PST no increase of gluconeogenesis was observed. From these results, it can be concluded that an alpha 1-adrenergic agonist specifically stimulates renal gluconeogenesis in PCT, but not in PST.

Adrenergic alpha-Agonists↗
PubMed1986

Localization and properties of NAD-dependent 15 hydroxyprostaglandin dehydrogenase activity in spontaneously hypertensive rat kidney.

To evaluate the pathophysiological significance of renal NAD-dependent 15 hydroxyprostaglandin dehydrogenase (PGDH) in young spontaneously hypertensive rats (SHR), the intranephron distribution of PGDH was compared with age-matched Wistar Kyoto rats (WKY). With supernatants of kidney homogenates, PGDH activities in 3 week-old SHR were significantly lower than those in WKY, and no difference in PGDH activities was found between male and female in both WKY and SHR. By using microdissected nephron segments of 3 week-old WKY and SHR, PGDH activities in both groups were found to be exclusively distributed in the proximal tubules, within which the activity of the straight portion (PST) was several fold higher than that of the convoluted one (PCT). In 3 week-old SHR, a significant decrease of PGDH activity was observed only in PST, possibly indicating a decrease of enzyme content in PST because of similar Km values in both groups. These results may suggest that intraproximal PG concentration could be regulated by the change of PGDH in PST of young SHR.

Animals↗
PubMed1985

Atrial natriuretic peptides stimulate renal gluconeogenesis.

Atrial natriuretic peptide (5-28AA; ANP) and atrial extract (ANS) stimulated rat renal gluconeogenesis in cortical tubule suspension in a dose dependent fashion only from substrates that enter gluconeogenesis via phosphoenol-pyruvate carboxylase. The effects of ANP and ANS were significantly potentiated by cAMP and cGMP, whereas methoxamine showed no effect. Extracellular calcium revealed a key role for ANP and ANS response to gluconeogenesis: a concentration of calcium higher than 1 mM was essential. Isolated cells from cortex which lost cell membrane polarity by warming but responded solely to cAMP and cGMP showed no effect by ANP nor ANS. These data suggest that ANP or ANS may act mainly from the basolateral site in the proximal tubule cell and promote gluconeogenesis through cAMP and/or cGMP system.

Animals↗
PubMed1985

Localization and properties of NAD+-dependent 15-hydroxyprostaglandin dehydrogenase activity in the rat kidney.

Localization of NAD+-dependent (type I) 15-hydroxyprostaglandin dehydrogenase (15PGDH) in the rat kidney was examined using an ultramicro assay of the enzyme activity based on the enzymatic cycling method. The enzyme activities during first 3 weeks of age were 30- to 40-fold higher than the adult and rapidly decreased by 4th week. 15PGDH activities measured with either PGE2 or PGF2 alpha as a substrate were five times higher in slices from midcortical or juxtamedullary layers than in slices from the superficial cortex of 3 week-old rat kidney. Little activity was found in inner medulla and papilla. When the enzyme activity was assayed using isolated nephron segments dissected from collagenase treated slices of 3 week-old rat kidneys, the activity was localized only in the proximal convoluted and straight tubules with either PGs (PGE2: 1.75 +/- 0.25 in PCT, 7.70 +/- 1.19 in PST, and PGF2 alpha: 1.63 +/- 0.39, 6.18 +/- 1.52 pmoles NADH/mm/40 min). The kinetic analysis for renal 15PGDH of 3 week-old rats revealed that Km for PGE2 (8.4 microM) was lower than that for PGF2 alpha (22.6 microM) with constant NAD+, while Vmax for both was similar. In contrast, both Km and Vmax for NAD+ were identical with either PGs. These data suggest that the rate-limiting factor of type I 15PGDH is the concentration of prostaglandins in the kidney rather than the concentration of NAD+.(ABSTRACT TRUNCATED AT 250 WORDS)

Aging↗
PubMed1985

Effect of chronic metabolic acidosis on ammonia production from L-glutamine in microdissected rat nephron segments.

To evaluate the role of each nephron segment in renal ammoniagenesis, distribution of renal ammoniagenic activity along the nephron in control and acidotic rats was examined. We used our original aerobic incubation system and ammonia produced from glutamine in 7 defined segments of microdissected nephron was measured using the enzymatic cycling method. When ammonia production in the control was compared in each nephron segment, the highest specific activity of ammoniagenesis per mm tubular length and that per microgram protein were observed in the proximal straight tubule (PST) and the thick ascending limb of Henle's loop, respectively. Chronic metabolic acidosis increased ammonia production per mm tubular length markedly in the proximal convoluted tubule (PCT) (+171%), moderately in the medullary collecting tubule (+123%) and PST (+77%), and slightly in the distal convoluted tubule (+52%), revealing that the highest activity of ammoniagenesis was located in PCT and PST in acidosis. These data indicate that proximal tubules have major roles in renal ammoniagenesis both in the control and in acidosis. From the early observation of glutaminase I isoenzyme distribution along the nephron, our data suggest that not only phosphate-dependent glutaminase but also phosphate-independent glutaminase may have important roles in renal ammoniagenesis.

Acidosis↗
PubMed1983

Narcotic physical dependence and urinary sex-dependent low molecular weight proteins in male rats.

The relationship between urinary excretion of sex-dependent low molecular weight proteins (LMWP) in male rats and narcotic dependence is described in this study. Rats were intermittently infused with narcotics at one hour intervals through an implanted intravenous cannula. Development of physical dependence on morphine, pethidine, and pentazocine was detected by withdrawal signs including body weight loss and abnormal behaviors after naloxone challenge. In these animals, a significant decrease in urinary LMWP excretion was found following the second day of each drug treatment without significant changes in albumin excretion, and this decrease was observed continuously throughout the experiment. The markedly decreased level of LMWP recovered to the control level within 7 d after withdrawal of the drugs. These results suggest that the decrease in urinary excretion of sex-dependent LMWP in male rats is a phenomenon closely related to narcotic dependence.

Animals↗
PubMed1983

A new approach for assessment of narcotic physical dependence using urinary sex-dependent low molecular weight proteins in male rats.

Attempts have been made to examine the relationship between urinary excretion of sex-dependent low molecular weight proteins found only in male rats (LMWP) and morphine physical dependence. Chronic administration of morphine produced a dose-related decrease in urinary LMWP excretion, which was correlated to the intensity of withdrawal signs including body weight loss and abnormal behaviors recognized after naloxone challenge. Furthermore, a statistically high correlation was obtained between the decrease in urinary LMWP excretion and the loss of body weight precipitated by naloxone challenge. LMWP was identified immunologically in the livers, kidneys, and sera using an antibody against purified LMWP. The serum level of LMWP was increased rapidly following bilateral nephrectomy. After chronic treatment with morphine, the LMWP content in the livers, kidneys, and sera were decreased. These findings indicate that the decrease in urinary LMWP excretion induced by chronic administration of morphine can be a useful parameter to assess the development of physical dependence on narcotics on the peripheral level without requiring drug withdrawal and naloxone challenge. This decrease in urinary LMWP may be caused by the inhibition of LMWP synthesis in the liver.

Animals↗
PubMed1983

Cytochrome P-450 monooxygenase system in the rabbit kidney: its intranephron localization and its induction.

Two components of the renal cytochrome P-450 (P-450) monooxygenase system, P-450 and NADPH-cytochrome c (cyt. c) reductase, were estimated using rabbit kidney slices and isolated nephron segments. Renal P-450 was distributed in the mitochondrial and microsomal fractions of both slices and nephron segments. P-450 (mitochondrial plus microsomal) was localized exclusively in the proximal tubule, with the highest activity in the S2 portion (18.14 +/- 5.47 fmoles/mm, 134.4 fmoles/micrograms protein). Intraperitoneal injection of 3,4-benzo(a)pyrene (BP) induced a 2-fold increase of only the microsomal P-450. The intraproximal site of BP action was localized in a definite portion, a segment 3 to 6 mm distant from the glomerulus (49.0 +/- 7.7 to 103.9 +/- 3.5 fmoles/micrograms protein), suggesting that inducible P-450 molecules may be enriched in this portion. Multiplicity of renal P-450 could be demonstrated electrophoretically. Comparison of the pattern from BP treated rabbits with control hemeprotein indicated that BP induced a higher molecular weight P-450. The highest concentrations of NADPH-cyt. c reductase were distributed in the cortical microsomes, although it was also detectable in the papilla. The reductase was distributed along the entire single nephron, with highest concentrations in the S2 portion of the proximal tubule. In conclusion, the P-450 monooxygenase system is localized in the proximal tubule and in the control condition, the highest activity is found in the S2 portion.

Animals↗
PubMed1983

Effects of starvation on microsomal cytochrome P-450 and laurate-omega-hydroxylation of rat kidney and liver.

Cytochrome P-450 (P-450) content and laurate-omega-oxidation activity in rat kidney and liver microsomes were investigated following starvation. Multiple forms of P-450 were analyzed by one dimensional separation using peroxidase stained SDS-continuous gradient polyacrylamide gel electrophoresis. Gels of the hepatic microsomes treated with phenobarbital showed three P-450 bands, and the renal microsomes showed one sharp band, which was induced remarkably by starvation and coincided with the middle molecular form of P-450 from the hepatic microsomes. Since laurate-omega-oxidation activity was induced specifically by starvation but not by drug treatment, in both the kidney and the liver microsomes, the middle molecular form of P-450 might catalyze laurate-omega-oxidation. It seemed, therefore, that a special P-450 subunit catalyzing laurate-omega-oxidation has a greater function in the renal rather than hepatic microsomes because the specific laurate-omega-oxidation activity per starvation induced P-450 content was relatively similar in both the kidney and the liver.

Animals↗
PubMed1983

Distribution and some characteristics of cytochrome P-450 in the kidney.

Intrarenal distribution of cytochrome P-450 (P-450) was investigated with different segments of isolated single nephrons from rabbits and rats by using a new ultra-micro method of P-450 determination. In both animals, P-450 was localized only in the proximal tubule. Other segments such as the glomerulus, the loop of Henle, the distal tubule, and the collecting tubule possessed no P-450 at all. Within the proximal tubule, the straight portion (S2 and/or S3 segments) revealed a higher specific content of P-450 than the convoluted one. An inducer of P-450, 3, 4-benzo(a)pyrene increased the P-450 of a definite portion (second 3 mm from the glomerulus) almost doubly in rabbits. In rats, both 3-methylcholanthrene (3MC) and 48 hr starvation (Fast) induced P-450, but only the later increased laurate-omega-hydroxylation. P-450 in the proximal convoluted and straight tubules was induced separately by Fast and 3MC, respectively. These results indicate that renal mixed function oxidase should be confined to the proximal tubule and that, like the liver, multiple forms of renal P-450 should exist in the different proximal segments.

Animals↗
PubMed1983

[Relationship between the decrease in urinary sex-dependent low molecular weight proteins by morphine and hormonal parameters in male rats].

The relationship between the decrease in urinary sex-dependent low molecular weight proteins (LMWP), which exist only in the male rat, and the serum levels of some hormones were examined in this study. Castration of male rats reduced the urinary excretion of LMWP by about 50%. Replacement therapy with testosterone increased the urinary LMWP excretion. Adrenalectomy did not affect the urinary excretion of LMWP. In the adrenalectomized rat, however, corticosterone increased LMWP excretion. Therefore, it is considered that testosterone and corticosterone play a part in the urinary excretion of LMWP under physiological conditions and that the effect of testosterone is more specific than that of corticosterone. Serum concentration of testosterone and corticosterone tended to increase in comparison with the control on the 7th day after chronic treatment with morphine (0.5 mg/g food), when the urinary excretion of LMWP was significantly decreased. Furthermore, after rats were chronically administered morphine following castration or adrenalectomy, the urinary LMWP excretion was markedly decreased in the same way as found in intact animals. On the other hand, the serum thyroxine level of rats treated with morphine for 7 days was significantly lower than that of the control. Thyroxine increased dose-dependently the decreased urinary excretion of LMWP induced by morphine administration. These findings suggest that the decrease in urinary excretion of LMWP after chronic treatment with morphine may be caused by the change of serum thyroxine level via the action of morphine on the endocrine functions.

Adrenalectomy↗
PubMed1983

Urinary sex-dependent low molecular weight proteins as a sign of narcotic dependence in male rats.

The relationship between urinary excretion of sex-dependent low molecular weight proteins (LMWP) in male rats and narcotic dependence has been investigated in this study. Chronic administration of codeine (0.5 mg/g food) caused a significant decrease in urinary excretion of LMWP from the third day, without any change in urinary high molecular weight proteins. The decrease recovered to the control level after the withdrawal of codeine. Withdrawal symptoms including loss of body weight and diarrhea were observed following codeine withdrawal. In animals chronically treated with pethidine (1.0 mg/g food), however, neither changes in urinary LMWP excretion nor withdrawal symptoms were observed. These present findings suggest that the decrease in urinary excretion of sex-dependent LMWP is related to narcotic dependence in male rats, since we previously reported the decrease in urinary excreted LMWP in morphine-dependent rats.

Albuminuria↗