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  • 1
    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
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Pflügers Archiv 405 (1985), S. 170-172 
    ISSN: 1432-2013
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract To examine the role of Na-K-ATPase in the natriuresis that occurs after acute extracellular volume expansion, we performed acute clearance experiments and in vitro analysis of renal microsomal ATPase activity in rats receiving intravenous 0.9% sodium chloride (0.1 ml/100g bw/min). Despite increased absolute reabsorption of filtered sodium (196±8.1 vs. 165±11.4 uEq/min, p〈0.05), renal medullary microsomal Na-K-ATPase activity was decreased from 134±5.9 to 110±6.3 pmol Pi/mg protein/hour (p〈0.02). No changes occurred in cortical or papillary regions and Mg-ATPase was unaffected. Similar results were obtained after adding 4 mEq/l potassium chloride to the infusion to prevent any fall in serum K+. These data suggest that a considerable percentage of sodium reabsorption is suppressed in acutely volume expanded animals and it is proposed that this is mediated by inhibition of medullary Na-K-ATPase.
    Type of Medium: Electronic Resource
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  • 3
    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
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  • 4
    Electronic Resource
    Electronic Resource
    Springer
    Pflügers Archiv 352 (1974), S. 47-59 
    ISSN: 1432-2013
    Keywords: Kidney ; ATPase ; Transport ; Cortex ; Medulla ; Papilla
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary 1. The properties of microsomal ATPase were compared in the cortex, medulla and papilla of the rat kidney. 2. Activation of (Na+K)-dependent ATPase in the medulla was at lower potassium concentration than in the cortex or papilla. 3. (Na+K)-dependent ATPase in the papilla was more sensitive to ouabain than cortical or medullary ATPase. 4. (Na+K)-dependent ATPase in the kidney papilla was more sensitive to inhibition by calcium, cadmium andN-ethyl-maleimide than the enzyme from the kidney cortex or medulla. 5. Mg-ATPase in each region of the kidney was more resistant to inhibition by calcium, cadmium orN-ethyl-maleimide than the corresponding (Na+K)-dependent activity. 6. Mg-ATPase in the papilla was more resistant to inhibition by these inhibitors as well as by thiocyanate than the enzyme from cortex or medulla. 7. These data may suggest functional differences in the microsomal ATPase of various regions in the kidney.
    Type of Medium: Electronic Resource
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  • 5
    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
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  • 6
    Electronic Resource
    Electronic Resource
    Springer
    Pflügers Archiv 394 (1982), S. 165-173 
    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.
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  • 7
    Electronic Resource
    Electronic Resource
    Springer
    Pflügers Archiv 345 (1973), S. 81-92 
    ISSN: 1432-2013
    Keywords: Urea ; Sodium ; Kidney ; Transport ; (Na+K)-ATPase
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Microsomal ATPase activity was studied in three regions of the rat kidney: cortex, medulla and papilla. (Na+K)-ATPase activity was highest in the medulla but a substantial activity, comparable to that in the cortex, was also present in the papilla. In the presence of high sodium (200–320 mM) or urea (100–900 mM) progressive inhibition of Mg-ATPase activity was observed in all three regions of the kidney. Urea (900 mM) or Na (320 mM) caused activation of (Na+K)-dependent ATPase in the medulla and inhibition of this enzymatic activity in the papilla of the kidney. Total microsomal ATPase activity in the medulla was unchanged in the presence of urea or sodium but was reduced in the papilla. Urea inhibited non-selectively Mg-p-nitrophenylphosphatase and K-activated p-nitrophenylphosphatase in all three parts of the kidney. These findings may point to a molecular basis for the function of urea and of sodium in the concentrating mechanism of the kidney.
    Type of Medium: Electronic Resource
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  • 8
    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
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  • 9
    Electronic Resource
    Electronic Resource
    Springer
    Pflügers Archiv 398 (1983), S. 247-252 
    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
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  • 10
    ISSN: 1432-2013
    Keywords: Genetic hypertension ; Rats ; Water handling ; Anti-diuretic hormone
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The renal handling of water by SBH and SBN rats was evaluated under basal conditions and following various intervention procedures. During 17 weeks of unrestricted water intake, SBH rats drank less water and excreted less urine with a higher osmolality than SBN. The differences in urine volume and osmolality persisted during 2 weeks of paired water intake. Acute water loading elicited comparable dilution of the urine in the two strains. Water deprivation for 48 h resulted in a marked rise in urine osmolality, which tended to be higher in SBN. Administration of exogenous vasopressin in water loaded animals caused a similar rise in urine osmolality. Papillary solute and urea content was higher in SBH than in SBN, but comparable in water loaded animals. The results show that although SBH differ from SBN rats in the handling of water under basal conditions, their renal diluting and concentrating capacity is comparable at extreme conditions. GFR and RBF were equal in both strains. The data suggest that SBH rats have increased renal water reabsorption as compared to SBN, which may be mediated by ADH, PG or other mechanisms. This characteristic may be related to their propensity to develop hypertension.
    Type of Medium: Electronic Resource
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