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PubMed1995

Suppressed expression of calcium-binding protein regucalcin mRNA in the renal cortex of rats with chemically induced kidney damage.

The alteration of Ca(2+)-binding protein regucalcin mRNA expression in the kidney cortex of rats administered cisplatin and cephaloridine, which can induce kidney damage, was investigated. Cisplatin (0.25, 0.5 and 1.0 mg/100 g body weight) or cephaloridine (25, 50 and 100 mg/100 g) was intraperitoneally administered in rats, and 1, 2 and 3 days later they were sacrificed. The alteration in serum findings after the administration of cisplatin (1.0 mg/100 g) or cephaloridine (50 and 100 mg/100 g) demonstrated chemically induced kidney damage; blood urea nitrogen (BUN) concentration increased markedly and serum inorganic phosphorus or calcium concentration decreased significantly. Moreover, the administration of cisplatin (1.0 mg/100 g) or cephaloridine (100 mg/100 g) caused a remarkable increase of calcium content in the kidney cortex of rats, indicating kidney damage. The expression of regucalcin mRNA in the kidney cortex was markedly reduced by the administration of cisplatin or cephaloridine in rats, when the mRNA levels were analyzed by Northern blotting using rat liver regucalcin cDNA (0.9 kb). The mRNA decreases were seen with the used lowest dose of cisplatin or cephaloridine. The present study clearly demonstrates that the mRNA expression of Ca(2+)-binding protein regucalcin in the kidney cortex of rats is decreased by chemically induced kidney damage.

Animals↗
PubMed1978

[In vivo determination of local tissue pO2 in renal cortex in kidney transplantation].

From measurement of local tissue PO2 in human kidney grafts after restoration of renal circulation, a correlation between initial microcirculation and kidney function can be drawn. PO2-histograms of kidney grafts with sufficient function are normal, whereas PO2-histograms of kidneys with delayed onset of function (congruent to 3 weeks) show distinct disturbances of microcirculation. These preliminary results suggest that measuring local tissue PO2 in transplanted kidneys may be of value for the prognosis of the graft.

Humans↗
PubMed1978

Sterol synthesis and CO2 production from mevalonate in calves.

Nonruminating male Holstein calves were fed a reconstituted milk containing 11.7% nonfat-dried-milk solids and 3.5% beef tallow. Calves were slaughtered at 17 weeks of age. Samples of perirenal adipose tissue, liver, muscle, small intestine, kidney cortex, and kidney medulla were assayed in vitro for sterol synthesis and production of (14)CO(2) from [2-(14)C]mevalonate. Of the tissues tested, adipose tissue and kidney medulla produced nonsaponified lipids at the greatest rates; kidney cortex and liver at half the rate of adipose tissue; muscle and jejunum at one-eighth the rate of adipose tissue; and ileum at a negligible rate. The amount of (14)C in squalene, lanosterol, and cholesterol of the nonsaponified lipids of each tissue was determined by thin-layer chromatography. Proportions of (14)C in cholesterol to (14)C in total nonsaponified lipids ranged from 30% to 59%; squalene, from 5% to 27%; and lanosterol, from 11% to 59% of the total nonsaponified lipids present. The rate of CO(2) production by the "trans-methylglutaconate shunt of mevalonate metabolism" was determined. Kidney cortex displayed the greatest shunt activity, producing 15-80-fold more CO(2) than any other tissue tested. Ileum, jejunum, skeletal muscle, and kidney medulla had similar shunt activities; liver sections had less shunt activity, and no shunt activity was detected in adipose tissue. These data reveal a shunt for mevalonate utilization that does not lead to sterols and also show that the kidney is important in the sterol and nonsterol metabolism of mevalonate.

Adipose Tissue↗
PubMed1985

The in vitro formation of sulfates and glucuronides of estrogens by adult and fetal ovine tissues.

Incubation of nanomolar concentrations of [3H]estrone with ovine liver slices from adult and fetal animals demonstrated, in particular, the production of estrogen sulfates together with smaller amounts of glucuronides, even although microsomal estrogen glucuronyltransferase (GT) and sulfatase activities were high, especially in adult tissue. [3H]Estriol was conjugated almost exclusively as sulfate under the same experimental conditions. Slices of maternal and fetal kidney medulla were also strikingly active in promoting estrogen sulfate production as were slices of fetal kidney cortex. Adult kidney cortex conjugated estrogen only in the glucuronide form. These data indicate the possibility that maternal and fetal liver and kidney might contribute to the high circulating level of estrone sulfate in the pregnant sheep. Through the use of [3H]estrone and [3H]estrone sulfate as substrates, it was possible to demonstrate that adult slices of kidney medulla possessed relatively low sulfatase, considerable sulfotransferase (ST), and virtually no GT activity, whereas cortex had high sulfatase, little or no ST, and low, though demonstrable, GT activity. The ST activity of kidney high-speed supernatants was stimulated by the presence of sulfhydryl groups, whereas that in liver was not. Enzymic reduction of estrone and (or) estrone sulfate by liver and kidney slices indicated that, in the former, 17 alpha-reduction prevailed and, in the latter with the exception of the maternal medulla, 17 beta-reduction was the main pathway, particularly in the fetus.

Animals↗
PubMed1993

Cloning and expression of a rabbit cDNA encoding a serum-activated ethylisopropylamiloride-resistant epithelial Na+/H+ exchanger isoform (NHE-2).

A unique Na+/H+ exchanger isoform, NHE-2, was cloned and characterized. NHE-2 is a protein of 809 amino acids with a calculated size of 90,787. It exhibits overall amino acid identity of 50, 44, and 60% with other cloned mammalian Na+/H+ exchangers NHE-1, NHE-3, and NHE-4, respectively. Northern blot analysis of poly(A+) RNA isolated from rabbit ileum, kidney cortex, and kidney medulla using NHE-2 cDNA as a probe revealed messages of 5.2, 4.2, and 3.2 kilobases with relative abundance (in descending order) kidney medulla > kidney cortex > ileum. More detailed tissue distribution of message was performed by ribonuclease protection assay. NHE-2 was predominantly expressed in kidney, intestine, and adrenal gland with a small amount in skeletal muscle and trachea. Stable expression of NHE-2 in PS120 fibroblasts confirmed that NHE-2 is a functional Na+/H+ exchanger which is defined by amiloride-sensitive Na+-dependent alkalinization of acid-loaded cells. NHE-2 has the same Ki for amiloride inhibition as NHE-1 (1 microM) but is 25-fold more resistant to ethylisopropylamiloride inhibition than is NHE-1 (500 versus 20 nM). Like NHE-1, NHE-2 can be activated by serum. Expression of NHE-2 in a polarized human intestinal epithelial cell line, Caco-2 cells, results in functional expression of NHE-2 in the apical membrane. Thus, we conclude that NHE-2 is a candidate to be an apical membrane Na+/H+ exchanger in intestinal and renal epithelial cells.

Adenocarcinoma↗
PubMed1994

Plasma renin activity and changes in tissue angiotensin converting enzyme.

OBJECTIVES: Recent evidence suggests that tissue generation of angiotensins I and II depends on the level of the plasma components of the renin-angiotensin system and on tissue-specific processes. The present study was undertaken to clarify the possible relationship between plasma renin activity (PRA) and tissue angiotensin converting enzyme (ACE) activity in the heart, lung, kidney cortex and kidney medulla of Wistar-Kyoto rats. In the kidney cortex particular attention was focused on renal brush-border ACE. METHODS: Different experimental models known to have opposite effects on PRA were used: changes in salt intake, deoxycorticosterone acetate (DOCA) with or without salt supplements, and the Goldblatt two-kidney, one clip (2-K,1C) model. Two weeks after the start of the experiments the rats were killed, and PRA, and plasma and tissue ACE activity, were measured. RESULTS: At the end of the study the blood pressure in the treated rats was not significantly different from control. As expected, the PRA were highest in the 2-K,1C and depleted-salt groups and lowest in the DOCA, DOCA-salt and high-salt groups. ACE responses were different in different types of tissue, with no relationship between PRA and plasma or tissue ACE activity. For example, DOCA treatment led to increased ACE activity in the heart and the kidney only if the rats were maintained on a high salt intake. DOCA or salt alone failed to have this effect. In the 2-K,1C model the unclipped kidneys did not show any significant variation in ACE activity, but the clipped kidneys exhibited increased ACE activity compared with sham-operated rats. This increase, coupled with increased renal renin secretion, could play a role in the acceleration of local angiotensin II formation, and could thus initiate and sustain the development of hypertension in this model. CONCLUSION: The present results show that variations in ACE activity were organ-specific and were not linked either to hypertension or to changes in PRA.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1988

Postmortem biochemical indices of antemortem hemorrhagic shock.

The purpose of this study was to determine if the perturbations in two glycolytic metabolites that occur during hemorrhagic shock can be used as discriminatory postmortem indicators of death resulting from severe hemorrhagic shock. Two groups of male albino Sprague-Dawley rats were hemorrhaged by withdrawing either 40% (Group I) or 45% (Group II) of the total blood volume. Glycogen and lactate concentrations were determined at 0 and 48 hr postmortem in the following tissues and organs: diaphragm, heart, liver, kidney cortex, and kidney medulla. The differences in lactate and glycogen in Group I at 0 hr were not significantly different from the nonhemorrhaged controls, with the exception of the lower liver glycogen concentration (58% of control). In Group II glycogen concentration was significantly reduced at 0 hr in the diaphragm (70% of control), liver (37%), and kidney medulla (55%). Lactate concentration was higher in all tissues examined by 270-640%; within 48 hr all tissues for both control and hemorrhaged animals had declined to baseline levels of glycogen concentration, whereas lactate levels had increased as much as 34-fold. There were no highly significant differences in glycogen at 48 hr between the control and hemorrhaged groups. In Group II the lactates were similar for both the control and hemorrhaged animals with the exception of the higher concentrations in the kidney cortex (54%) and medulla (41%). It was concluded from these findings that although significant metabolic perturbations are present at the time of death due to hemorrhage these differences do not persist up to 48 hr postmortem, with the possible exception of the kidney lactate concentrations.

Animals↗
PubMedDate not supplied

[Effect of disconnection of various types of autonomic mediation on the adenyl system of the cortex of a solitary kidney].

The authors studied the ATP, ADP, and AMP intratissue content and the energy charge of the kidney cortex in compensatory hypertrophy during a continuous blocking effect produced by daily guanethidine and atropine injections on the transsynaptic mechanisms of sympathetic and parasympathetic neuromediation. Chronic disorders of energy metabolism were noted in both groups, which were more marked in deparasympathization. Complex combinations of the constant functional load exerted on the organ with the metabolic effects of the mediatory block in the tissues and disorders of their blood supply are the causes of tissue energy deficiency. The disorders of energy metabolism in the late periods of the experiment (after 60 days) in both cases were caused by deterioration of the blood supply to the cortex due, probably, to the noted accumulation in the tissue of metabolites of macroergic compounds which are vasoconstrictors of the renal arterioles.

Adenine Nucleotides↗
PubMed1991

Opioid binding sites in the guinea pig and rat kidney: radioligand homogenate binding and autoradiography.

The specific binding of the selective mu-, delta-, and kappa-opioid ligands [3H][D-Ala2,MePhe4,Gly-ol5]enkephalin ([3H] DAGOL), [3H][D-Pen2,D-Pen5]enkephalin ([3H]DPDPE), and [3H]U69593, respectively, to crude membranes of the guinea pig and rat whole kidney, kidney cortex, and kidney medulla was investigated. In addition, the distribution of specific 3H-opioid binding sites in the guinea pig and rat kidney was visualized by autoradiography. Homogenate binding and autoradiography demonstrated the absence of mu- and kappa-opioid binding sites in the guinea pig kidney. No opioid binding sites were demonstrable in the rat kidney. In the guinea pig whole kidney, cortex, and medulla, saturation studies demonstrated that [3H]DPDPE bound with high affinity (KD = 2.6-3.5 nM) to an apparently homogeneous population of binding sites (Bmax = 8.4-30 fmol/mg of protein). Competition studies using several opioid compounds confirmed the nature of the delta-opioid binding site. Autoradiography experiments demonstrated that specific [3H]DPDPE binding sites were distributed radially in regions of the inner and outer medulla and at the corticomedullary junction of the guinea pig kidney. Computer-assisted image analysis of saturation data yielded KD values (4.5-5.0 nM) that were in good agreement with those obtained from the homogenate binding studies. Further investigation of the delta-opioid binding site in medulla homogenates, using agonist ([3H]DPDPE) and antagonist ([3H]diprenorphine) binding in the presence of Na+, Mg2+, and nucleotides, suggested that the delta-opioid site is linked to a second messenger system via a GTP-binding protein. Further studies are required to establish the precise localization of the delta binding site in the guinea pig kidney and to determine the nature of the second messenger linked to the GTP-binding protein in the medulla.

Analgesics↗
PubMed1983

[Prostaglandin catabolism in the mammalian kidney--histochemical and electrophoretic studies].

Using the prostaglandins PGE2, PGF2 alpha and PGB1 as substrates for demonstration of NAD-15-PGDH activity and of 13,14,15-Keto-PGF2 alpha for demonstration of NAD-9-PGDH activity these enzymes were localized in native sections of rat kidney by membrane incubating technique. Both enzymes are active in the same tubular structures of kidney cortex. Simultaneously homogenate supernatant of kidney cortex was separated by micro-electrophoretic technique. NAD-15-PGDH exist in rat kidney in multiple forms, which are varied in number (1 to 3) during postnatal development. One or 2 fractions of NAD-9-PGDH are detected in rat kidney cortex. In the kidney cortex of rabbit and guinea pig also multiple forms of NAD-15-PGDH exist, but not in the kidney cortex of pig. No multiple forms of NAD-9-PGDH are detectable in the kidney of pig, guinea pig, and rabbit. The histochemical and electrophoretical results suggest an important relationship between prostaglandin catabolizing activity and nephrogenesis in the early development of rat kidney. The functional significance of the detected multiple forms of NAD-15-PGDH and the variation in the number of fractions during ontogenesis in rat kidney are yet not clear.

Animals↗
PubMed2000

Enalapril and captopril enhance glutathione-dependent antioxidant defenses in mouse tissues.

The effect of enalapril and captopril on total glutathione content (GSSG + GSH) and selenium-dependent glutathione peroxidase (Se-GPx) and glutathione reductase (GSSG-Rd) activities was investigated in mouse tissues. CF-1 mice (4-mo-old females) received water containing enalapril (20 mg/l) or captopril (50 mg/l) for 11 wk. Enalapril increased GSSG + GSH content (P < 0.05) in erythrocytes (147%), brain (112%), and lung (67%), and captopril increased GSSG + GSH content in erythrocytes (190%) and brain (132%). Enalapril enhanced Se-GPx activity in kidney cortex (42%) and kidney medulla (23%) and captopril in kidney cortex (30%). GSSG-Rd activity was enhanced by enalapril in erythrocytes (21%), brain (21%), liver (18%), and kidney cortex (53%) and by captopril in erythrocytes (25%), brain (19%), and liver (34%). In vitro erythrocyte oxidant stress was evaluated by thiobarbituric acid-reactive substances (TBARS) production (control 365 +/- 11, enalapril 221 +/- 26, captopril 206 +/- 17 nmol TBARS x g Hb(-1) x h(-1); both P < 0.05 vs. control) and phenylhydrazine-induced methemoglobin (MetHb) formation (control 66.5 +/- 3.5, enalapril 52.9 +/- 0.4, captopril: 56.4 +/- 2.9 micromol MetHb/g Hb; both P < 0.05 vs. control). Both angiotensin-converting enzyme inhibitor treatments were associated with increased nitric oxide production, as assessed by plasma NO-(3) + NO-(2) level determination (control 9.22 +/- 0.64, enalapril 13.7 +/- 1.9, captopril 17.3 +/- 3.0 micromol NO-(3) + NO-(2)/l plasma; both P < 0.05 vs. control). These findings support our previous reports on the enalapril- and captopril-induced enhancement of endogenous antioxidant defenses and include new data on glutathione-dependent defenses, thus furthering current knowledge on the association of ACE inhibition and antioxidants.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1982

[Histochemical determination of beta-hydroxybutyrate dehydrogenase in the brush border of the cortex epithelium of the rat kidney].

NAD-beta-hydroxybutyrate dehydrogenase activity was investigated in the kidneys of male and female adult Wistar rats using membrane incubating technique. In this connection the enzyme activity presents an other topochemical pattern as in comparison with conventional incubating technique. In the kidney cortex an additional reaction was demonstrated in the convoluted portion of proximal tubules. In connection with the results of biochemical investigations the soluble enzyme is characterized as a nonmitochondrial beta-hydroxybutyrate dehydrogenase of proximal kidney tubules (brush border membrane enzyme?).

Animals↗
PubMed1977

Release of free fatty acids by the rat kidney.

The authors studied the release of free fatty acids (FFA) by the rat kidney cortex. They found that the kidney cortex released FFA into the incubation medium like adipose tissue. The presence of Ca2+ ions did not affect FFA release. Glucose significantly inhibited it. It was further shown that the kidney cortex is sensitive to the akipokinetic action of adrenaline and the antilipolytic action of insulin, in the same way as adipose tissue. It is concluded from the results that the kidney cortex has a lipolytic system which seems to be subject to higher hormonal regulatory mechanisms.

Animals↗
PubMed2002

Apoptosis in the cortex of the developing mouse kidney.

Published levels of apoptosis in developing rat kidney (approximately 2.5%) seem large for a tissue with no obvious need for continual cell death. This paper examines the levels and patterns of apoptosis and mitosis in the cortical region of the developing metanephros of the mouse, the standard mammalian model embryo. Using confocal microscopy on specimens stained with propidium iodide to highlight nuclear morphology, optical sections of wholemount kidneys to a depth of approximately 50 microm were analysed and mitotic, apoptotic and interphase nuclei counted in the various compartments. Of the approximately 200 000 cells examined over E11.5-16.5, 2-3% were mitotic, confirming observations based on cryosections; the mitotic index peaked at E14.5, dropping to approximately 0.5% by P14. The mean apoptotic index during this period was 0.28%; this figure from wholemounts was approximately 10% of that earlier reported in cryosectioned rat kidneys. One possible explanation for the difference is that cryosectioning turns out to create small nuclear fragments that can stain strongly with propidium. Such fragments are not seen in wholemounts and do not stain with TUNEL. Wholemount mouse E11.5 tails and E16.5 lungs were also analysed and both their mitotic and their apoptotic indexes were similar to those in wholemount developing kidneys. These results show that the level of apoptosis in wholemount embryonic mouse kidney cortex is far less than previously reported in cryosectioned rat embryonic kidneys, and typical of that in other mouse embryonic tissues whose development seems not to require apoptosis.

Animals↗
PubMed1997

The formation of desethyl-piperacillin from piperacillin by human liver S9 in vitro.

Piperacillin (PIPC) has been used as one of the most useful beta-lactam antibiotics over the past 10 years. The metabolism of PIPC has been thoroughly investigated and it has been recognized that PIPC gives few metabolites in laboratory species or humans. Recently, an active metabolite, desethyl-piperacillin (DEt-PIPC), was detected in human plasma and urine after PIPC administration. In the current study, human tissues were obtained from organ donors (n = 3) and subcellular fractions (S9) were prepared. The time course of metabolism by S9 mix from liver, kidney cortex, and kidney medulla was then determined using 0.5 mM PIPC. For comparative purposes, rat liver S9 were also prepared and incubated with PIPC under the same conditions. DEt-PIPC was formed by human liver S9 mix from all three specimens studied, with the rate varying approximately eightfold. No DEt-PIPC was detected in any of the incubations with rat liver S9 mix (n = 3) and kidney S9 mix (n = 3) prepared from either the cortex or medulla. In summary, these data suggest that the formation of the unique human metabolite, DEt-PIPC, can be predicted by in vitro studies with human tissues and that this metabolite is formed predominantly by the liver.

Adult↗
PubMed1977

Metabolism in the hypothermically perfused dog kidney. Incorporation rate of leucine and threonine into proteins.

The incorporation of [14C]leucine and [14C]threonine into kidney cortex proteins was studied during 6 days' hypothermic perfusion of dog kidneys at 8-10 degrees C and during in vitro incubation of dog kidney cortex slices at 37 degrees C. Leucine carbon was incorporated into proteins at a higher rate than threonine carbon both during in vitro incubation of kidney cortex slices and during hypothermic kidney perfusion. The incorporation of leucine and threonine during hypothermic perfusion was linear for 6 days but 50-100 times lower than the incorporation of leucine and threonine in kidney cortex slices at 37 degrees C. During hypothermic perfusion there was a decrease in specific activity of leucine and threonine in the perfusate corresponding to a degradation of proteins which was greater than protein synthesis as calculated from the incorporation of label into proteins. Leucine carbon was recovered in CO2 during hypothermic perfusion and in vitro incubation of kidney cortex slices at 37 degrees C. The incorporation of threonine carbon into CO2 was about 10% of the corresponding value for leucine both during hypothermic kidney perfusion and during in vitro incubation of kidney cortex slices at 37 degrees C. It is concluded that there is a turnover of kidney proteins during hypothermic perfusion with a perfusate containing amino acids.

Amino Acids↗
PubMedDate not supplied

The hair-organ relationship in mercury concentration in contemporary Japanese.

The hair-organ relationship of mercury concentration was investigated in 46 autopsy samples in Tokyo, Japan. Hair mercury levels were highly significantly correlated with organ Hg levels in the cerebrum, cerebellum, heart, spleen, liver, kidney cortex, and kidney medulla, when the total mercury or methyl mercury value in the organ was compared with the hair total mercury or organic mercury, respectively. When the inorganic mercury value was tested, significant correlations remained, with weaker coefficients in all the organs but the spleen. Stepwise multiple regression analysis evidenced that the hair organic mercury value was the major explanatory variable for the organ total mercury or organ methyl mercury value in all the organs. To explain the organ inorganic mercury value, the hair organic mercury value was the major variable for the cerebrum and kidney (both cortex and medulla), the hair inorganic mercury value was the major variable for the cerebellum and heart, and the hair phosphorous and hair organic mercury were the major variables for the liver; no explanatory variable existed for the spleen. Auxiliary explanatory variables accounted for the organ total mercury and inorganic mercury levels, among which the hair selenium value was conspicuous with negative regression coefficients.

Adolescent↗