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  • 1
    Electronic Resource
    Electronic Resource
    The effect of 24,25 dihydroxyvitamin D3 on calcium efflux: the role of protein kinase C (1998)
    Oxford, UK : Blackwell Publishing Ltd
    Nephrology 4 (1998), S. 0 
    Details
    ISSN: 1440-1797
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: SUMMARY: 24,25 dihydroxyvitamin D3 (24,25(OH)2D3) is more abundant than 1,25(OH)2D3 in the serum. 1,25 dihydroxyvitamin D3, a potent calciotropic metabolite of vitamin D, has been shown to induce calcium efflux from bone. This action is probably mediated, in part, by protein kinase C (PKC). to determine whether 24,25(OH)2D3 affects calcium flux in bone, neonatal rat calvaria were cultured and the effect of 24,25(OH)2D3 on calcium flux and signal transduction pathways were evaluated. Compared with a control, 24,25(OH)2D3 (108 mol/L) inhibited basal net calcium efflux. 24,25 dihydroxyvitamin D3 also inhibited net calcium efflux induced by the phorbol ester 12 Myristate 13-Acetate (PMA). Translocation of PKC from the membrane to the cytosolic fraction was rapidly and transiently induced by 24,25(OH)2D3. However, 24,25(OH)2D3 had no effect on cyclic AMP (cAMP) production. In conclusion, 24,25(OH)2D3 has a direct effect on bone by inhibiting net calcium efflux which is probably mediated by the deactivation of PKC.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1440-1797.1998.d01-26.x
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  • 2
    Electronic Resource
    Electronic Resource
    Halothane hepatitis with renal failure treated with hemodialysis and exchange transfusion (1974)
    Springer
    Surgery today 4 (1974), S. 212-215 
    Details
    ISSN: 1436-2813
    Keywords: halothane hepatitis ; renal failure ; hemodialysis ; exchange transfusion
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract A 38-year-old white female, hepatitis B antigen negative, developed fluminating hepatic failure associated with oliguria and severe azotemia after two halothane anesthesia and without exposure to other hepatotoxic drugs or blood transfusions. She was treated with multiple hemodialysis and exchange blood transfusion. The combined treatment corrected the uremic abnormalities and improved her level of consciousness. The liver and kidney function gradually improved, and she made a complete recovery, the first recorded with hepatic and renal failure under these post-anesthetic conditions. Further evaluation of this combined treatment used for this patient is warranted.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02469454
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  • 3
    Electronic Resource
    Electronic Resource
    Sodium handling by the Sabra hypertension prone (SBH) and resistant (SBN) rats (1986)
    Springer
    Pflügers Archiv 407 (1986), S. 547-551 
    Details
    ISSN: 1432-2013
    Keywords: Genetic hypertension ; Doca-salt ; Sodium excretion ; Salt loading
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The acute and chronic renal handling of salt was evaluated in age matched Sabra hypertension-prone (SBH) and hypertension-resistant (SBN) rats. Acute oral (4 ml/100 g) and intravenous (3.3 ml/100 g) isotonic saline loading in unanesthetized normotensive animals maintained on normal diet elicited a significantly lesser diuretic and natriuretic response in SBH than in SBN. Intermittent studies in metabolic cages in rats aged 5 to 21 weeks showed that both strains consumed similar amounts of salt but that SBH excreted significantly less urinary sodium than SBN (F=40,p〈0.001). Twenty four hour clearance studies showed a similar filtered sodium load in the two strains but a lower total and fractional sodium excretion in SBH, suggesting increased tubular reabsorption. Under conditions of water diuresis, free water clearance was similar in the two strains, suggesting the site for disparate tubular sodium handling to be distal to the thick medullary ascending limb of the loop of Henle. Acute oral saline loading and long term studies in metabolic cages in rats prepared with deoxycorticosteroneacetate (doca) and salt showed no significant differences in sodium excretion between hypertensive SBH and normotensive SBN. These findings indicate disparate renal sodium handling between SBH and SBN rats, already apparent before the onset of hypertension, which dissipates during doca-salt treatment.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00657514
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  • 4
    Electronic Resource
    Electronic Resource
    The in vivo and in vitro effect of calmodulin antagonists on the renal actions of 25(OH) vitamin D3 in the rat (1989)
    Springer
    Pflügers Archiv 415 (1989), S. 372-380 
    Details
    ISSN: 1432-2013
    Keywords: Phosphaturia ; Parathyroid hormone ; 25 Hydroxy-vitamin D3 ; Trifluoperazine ; Adenylate cyclase ; Rat
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Previous work from this laboratory has demonstrated that 25(OH) vitamin D3 [25(OH)D3] acutely suppresses the phosphaturic action of parathyroid hormone (PTH) and interferes with the PTH-induced activation of adenylate cyclase (AC). Calmodulin inhibitors block vitamin D-induced Ca2+ transport in the gut and phosphorus uptake in renal BBMV's. We have examined whether calmodulin antagonists affect the renal action of 25(OH)D3. Acute clearance experiments were performed in PTH-infused parathyroidectomized rats receiving 25(OH)D3 after pretreatment with trifluoperazine (TFP) or promethazine (P). In vitro PTH-induced activation of renal AC was also studied in membrane preparations from pretreated rats in the presence of 25(OH)D3. 25(OH)D3 reduced the PTH-stimulated increase in fractional excretion of phosphorus (CP/CIn) from 0.292±0.024 to 0.195±0.018 (p〈0.005) and urinary cAMP from 149.3±20.3 to 78.1±10.4 pmol/min (p〈0.01) and also blunted AC activation in vitro. TFP but not P abolished the effects of 25(OH)D3 both in vivo and in vitro. R 24571 also abolished the in vitro effect of 25(OH)D3. Thus, (1) TFP abolishes both the antiphosphaturic and the AC/cAMP-related actions of 25(OH)D3, (2) P does not have these effects, and (3) R 24571 abolishes the in vitro effect of 25(OH)D3. These results suggest that the antiphosphaturic effect of 25(OH)D3 acting via the AC/cAMP system may be calmodulin dependent.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00370890
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  • 5
    Electronic Resource
    Electronic Resource
    Renal function and Na−K-ATPase in rats after suprarenal ligation of inferior vena cava (1982)
    Springer
    Pflügers Archiv 394 (1982), S. 165-173 
    Details
    ISSN: 1432-2013
    Keywords: Medullary Na−K-ATPase ; Suprarenal caval ligation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract To assess the effects of altered renal function on Na−K-ATPase, the following groups of rats were studied: 1. rats with suprarenal vena cava ligation (SVCL), la. DOCA-treated rats with SVCL, 2. rats with infrarenal vena cava ligation (IVCL), 3. rats with glycerol-induced acute renal failure, 4. rats with bilateral ureteric ligation, and 5. K-exalate-treated rats with SVCL. In group 1, acute renal failure with hyperkalemia developed and medullary Na−K-ATPase increased from 95±5 in control to 155±7 μmol Pi/mg prot//h,P〈0.001, DOCA did not prevent the increase of Na−K-ATPase. In group 2, medullary Na−K-ATPase decreased from 130±10 in control to 88±7,P〈0.01, in rats with IVCL. In group 3, cortical Na−K-ATPase decreased from 55±5 to 27±6,P〈0.02. In group 4, Na−K-ATPase was unchanged. In group 5, maintenance of normokalemia prevented the rise in Na−K-ATPase. These experiments demonstrated a K-dependent activation of medullary Na−K-ATPase after SVCL but not in other forms of renal failure. Because SVCL diminishes drastically GFR per nephron, the present findings imply that increased loads of Na and K per nephron are not a prerequisite for an increase in medullary Na−K-ATPase. Hyperkalemia in presence of increased renal venous pressure seems to be causually related to the rise in medullary Na−K-ATPase activity.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00582920
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  • 6
    Electronic Resource
    Electronic Resource
    Evidence for interference of vitamin D with PTH/PTHrP receptor expression in opossum kidney cells (1998)
    Springer
    Pflügers Archiv 436 (1998), S. 289-294 
    Details
    ISSN: 1432-2013
    Keywords: Key words Opossum kidney cells ; Parathyroid hormone cAMP ; Intracellular Ca2+ concentration ; 1 ; 25-Dihydroxy-vitamin D3 ; PTH/PTHrP receptor mRNA
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract  Vitamin D counters the phosphaturic action of parathyroid hormone (PTH) in rats in vivo. The present study was undertaken to examine this interaction using monolayers of Opossum kidney (OK) cells. 32P uptake, cAMP generation, PTH/PTHrP receptor mRNA expression and intracellular Ca2+ [Ca2+]i were measured in (1) control cells, (2) cells exposed to PTH, (3) cells pretreated with 1,25-dihydroxyvitamin D3 [1,25(OH)2D3], and (4) 1,25(OH)2D3-pretreated cells exposed to PTH. 32P uptakes were in (1) 5.00±0.20 (mean ±SE), in (2) 2.30±0.14 (P〈0.001 versus group 1), in (3) 4.80±0.24 (P NS versus group 1) and in (4) 3.70±0.20 (P〈0.001 versus group 2) nmol Pi/(mg·prot 10 mm). cAMP levels were in (1) 10±3, in (2) 210±8, in (3) 12±4, and in (4) 122±12 pmol cAMP/mg protein (P〈0.001 versus group 2). PTH/PTHrP receptor mRNA expression was in relative units: (1) 100±0, (2) 99.5±6.2, (3) 68.7±2.6 (P〈0.001 versus group 1), and (4) 34.8±3.3 (P〈0.001 versus group 1). In groups 2 and 4 PTH induced equal transient increments in [Ca2+]i. These experiments demonstrate that the effect of vitamin D on phosphate transport is associated with a commensurate diminution in PTH/PTHrP receptor gene expression and PTH-induced cAMP formation but not with Ca2+ transients. Vitamin D per se does not affect 32P uptake or cAMP generation while it slightly decreased PTH/PTHrP receptor gene expression. These observations demonstrate that: (1) 1.25(OH)2D3 directly antagonizes the effects of PTH on 32P uptake in OK cells, (2) this effect is mediated via inhibition of PTH-induced activation of AC/cAMP system, (3) the diminution in PTH-induced cAMP formation may stem at least in part from a decrease in the expression of PTH/PTHrP receptor mRNA.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004240050634
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  • 7
    Electronic Resource
    Electronic Resource
    The effect of streptozotocin-induced diabetes mellitus on urinary excretion of sodium and renal Na+−K+-ATPase activity (1984)
    Springer
    Pflügers Archiv 401 (1984), S. 97-100 
    Details
    ISSN: 1432-2013
    Keywords: Na−K-ATPase ; Streptozotocin ; Diabetes mellitus
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Renal sodium handling and microsomal Na+−K+-ATPase activity in kidney cortex, medulla and papilla of rats with streptozotocin-induced diabetes mellitus (DM) was studied. During 7 days following the administration of streptozotocin GFR, urinary excretion, filtered load and tubular reabsorption of Na+ averaged (mean±SE) 1.18±0.016 ml/min, 1.74±0.14, 177.3±8.9 and 175.6±8.9 mEq/min respectively in experimental rats as compared to corresponding rates of 0.85±0.04 (P〈0.001), 0.85±0.03 (P〈0.001), 129.8±5.8 (P〈0.001) and 129±5.8 (P〈0.001) respectively in the control rats. The activity of microsomal Na−K-ATPase in the kidney cortex, medulla and papilla of the control group was (mean±SE) 44.7±1.7, 150±7.5 and 37.4±3.6 (μmoles Pi/mg prot/h) respectively. 24 h after DM induction Na−K-ATPase activity in the cortex rose to 59.3±2.4 (P〈0.001) and remained high after 3 and 7 days. Medullary Na−K-ATPase activity was unchanged 24 h after streptozotocin administration but was markedly increased to 260±9 (P〈0.001) after 3 days and remained high after 7 days. These findings show that stretozotocin-induced DM in rats causes a substantial increase in GFR which is associated with a net increase in filtered and reabsorbed load of Na+ and natriuresis. These alterations are accompanied by a marked increase in Na−K-ATPase activity in renal medulla and in the cortex.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00581539
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  • 8
    Electronic Resource
    Electronic Resource
    Blockade of the renal tubular effects of vitamin D by cycloheximide in the rat (1983)
    Springer
    Pflügers Archiv 398 (1983), S. 247-252 
    Details
    ISSN: 1432-2013
    Keywords: Vitamin D ; Parathyroid hormone ; Cycloheximide ; Phosphorus
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract To further characterize the mechanisms by which 25(OH)vitamin D3 (25(OH)D3) and 1.25(OH)2 vitamin D3 (1,25(OH)2D3) suppress the phosphaturic action of parathyroid hormone (PTH) we have studied the effects of cycloheximide (cyclohex), a protein synthesis inhibitor, on the interaction between PTH and vitamin D metabolites in parathyroidectomized (PTX) rats, both in vivo and in vitro experiments. In clearance studies PTX PTH-infused rats were pretreated with cyclohex 2 h before the administration of vitamin D. In control, PTX PTH-infused rats not pretreated with cyclohex, the administration of 25(OH)D3 and 1,25(OH)2D3 was associated with a fall in fractional excretion of phosphate (CP/CIN) from 0.30±0.05 to 0.16±0.02 and from 0.31±0.05 to 0.13±0.01 (P〈0.005) respectively. Cyclohex-pretreated PTX PTH-infused rats failed to respond to both 25(OH)D3 and 1,25(OH)2D3, and CP/CIN, which rose after PTH, remained 0.32±0.05 and 0.29±0.03 respectively. In vitro, both 25(OH)D3 and 1,25(OH)2D3 inhibited the PTH-induced activation of adenylate cyclase in the renal isolated membrane fractions. Pretreatment with cyclohex abolished this effect of vitamin D metabolites. These results show that cyclohex blocks the antiphosphaturic effects of both 25(OH)D3 and 1,25(OH)2D3 but does not alter the response to PTH. These findings are consistent with the possibility that the acute renal action of vitamin D depends on de novo synthesis of protein.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00657160
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  • 9
    Electronic Resource
    Electronic Resource
    Renal refractoriness to PTH in experimental Fanconi syndrome: Evidence for intact adenylate cyclase activation (1984)
    Springer
    Pflügers Archiv 402 (1984), S. 116-119 
    Details
    ISSN: 1432-2013
    Keywords: Fanconi syndrome ; Parathyroid hormones ; Adenylate cyclase
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Previous studies demonstrated renal refractoriness to parathyroid hormone (PTH) in maleate-induced Fanconi syndrome (FS) in rats. In membrane fraction of renal cortex of parathyroidectomized (PTX) rats with FS, PTH increased adenylate cyclase (AC) activity from a basal value of 7.4±0.6 (x±SE) to 16.8±3.5 pmoles cAMP/mg prot/min (P〈0.01), similar stimulation by PTH was observed in control incubation with normal kidneys. In membrane fraction of renal cortex of PTX rats incubated with maleate, PTH increased AC from 5.7±0.42 to 10.7±1.08 (P〈0.01) similar to control incubation without maleate. In cortical slices from PTX rates with FS incubated in vitro, PTH increased cAMP content only from 4.0±0.21 to 5.27±0.27 pmole cAMP/mg prot (P〈0.005), while in slices from the control group the increment by PTH was from 3.9±0.43 to 10.7±0.93 pmoles cAMP/mg prot (P〈0.001). For the difference in the increment between the control and FS group,P〈0.001. In cortical tissue of PTX rats with FS, PTH injection failed to increase cAMP content: basal value 7.4±0.8 and with PTH 9.2±0.8 pmole cAMP/mg prot (P NS), as compared with controls: basal value 9.5±0.5 and with PTH 23.8±1.6 (P〈0.001). ATP content of cortical slices fell from a control value of 2.3±0.18 in PTX rats to 1.0±0.14 nmol/mg prot in PTX rats with FS. These results show, (1) normal response to PTH stimulation of cortical AC from rats with FS, and (2) failure of PTH to enhance formation of cAMP in renal cortical tissue from rats with FS. These findings are consistent with an intact PTH receptor/AC system in maleate induced FS, but inability to increase cAMP production probably because of comprized cellular metabolism causing reduced ATP content.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00584840
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  • 10
    Electronic Resource
    Electronic Resource
    The ontogeny of the expression of K+ channel-like gene (CHIF) in the rat kidney papilla (1998)
    Springer
    Pediatric nephrology 12 (1998), S. 540-544 
    Details
    ISSN: 1432-198X
    Keywords: Key words: Kidney papilla ; Ontogeny ; Ion transport ; Potassium channels ; CHIF
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract. Recently, an IsK-like potassium (K+) channel corticosteroid-induced gene (CHIF) was cloned. A high-K+ diet enhances, while a low-K+ diet decreases the expression of this gene. The major expression of CHIF in the adult rat kidney is in the papilla, where it is constitutive, in contrast to its inducibility by corticosteroids and a low-salt diet in the rat colon. In order to further understand the ontogeny of K+ clearance, we studied the presence of CHIF in the kidney papilla in different stages of rat development. Total RNA from rat kidney papillae of 1- to 3-day pre-labor unborn offspring, 2- to 3-day-old newborns, 10-day-old, 6-week-old, and 43-week-old rats underwent northern hybridization for CHIF and the α-subunit of the Na+-K+-ATPase mRNA. Minor expression of CHIF mRNA was found in fetal and newborn rat papillae, while older rats showed an age-related increase in gene expression1.The expression of the α-sub unit of the Na+-K+-ATPase was not age related. We conclude that CHIF is present in the rat kidney papilla and the expression is related to age. The relative deficiency of CHIF in the newborn may be one of the factors responsible for the reduced K+ clearance in is period.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004670050501
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