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Biomedical subjects

M M Popovtzer

Publications and source records attributed to M M Popovtzer.

At least 109 records · Page 6Linked to original sources
PubMed1985

The effect of acute saline volume expansion on renal Na-K-ATPase.

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/100 g bw/min). Despite increased absolute reabsorption of filtered sodium (196 +/- 8.1 vs. 165 +/- 11.4 uEq/min, p less than 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 less than 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.

Animals↗
PubMed1985

The effect of suppression of prostaglandin synthesis on renal function in rats with intact and reduced renal mass.

The present study was undertaken to assess the role of prostaglandin system in the compensatory response to reduced nephron population, respective to renal function and electrolyte excretion. Intact and 5/6 nephrectomized rats were divided in 4 groups: 1) rats pretreated with indomethacin, 2) rats pretreated with the vehicle of indomethacin, 3) rats pretreated with sulindac, and 4) rats pretreated with the vehicle of sulindac. In normal rats, indomethacin administration resulted in a mild decrease in creatinine clearance and a significant reduction of the urinary Na excretion. In the rats with reduced renal mass treated with indomethacin, the creatinine clearance did not differ from that in the control group. The 24 h urinary sodium excretion and the fractional excretion of sodium, however, were significantly lower in the indomethacin treated animals than in the control rats. No change in the creatinine clearance or in the sodium excretion was observed in all groups pretreated with sulindac. The urinary PGE2 and thromboxane excretion was significantly lower in the indomethacin treated intact rats and the rats with reduced renal mass. Sulindac induced a slight decrease in urinary excretion of PGE2 in intact rats. No significant change in urinary excretion of PGE2 or thromboxane was seen after sulindac in the rats with reduced renal mass. The antinatriuretic effect of indomethacin was dissociated from changes in urine flow in all groups of animals, suggesting that the increase in Na reabsorption took place in a water impermeable segment of nephron. These results suggest that the compensatory increase in urinary Na excretion per nephron in rats with reduced nephron population at least partly depends on an intact prostaglandin synthesis.

Animals↗
PubMed1985

The effect of acutely reduced plasma osmolality on acute renal failure in rats.

The present study was designed to evaluate the effect of acute fall in plasma osmolality in three models of acute tubular necrosis in rats: (a) glycerol, (b) arterial clamping and (c) mercuric chloride. Plasma osmolality was reduced by a water loading during a mild anaesthesia from 305 +/- 7 to 270 +/- 12 mosmol/kg of water (P less than 0.01). In the ischaemic models of acute tubular necrosis (glycerol and arterial clamping), during the first 24 h in rats with reduced plasma osmolality, the respective creatinine clearance rates (CCR), 0.04 +/- 0.02 and 0.06 +/- 0.04 ml/min, were strikingly lower than those in rats with normal osmolality, 0.21 +/- 0.03 and 0.26 +/- 0.06 ml/min (P less than 0.001) respectively. The control CCR were 0.65 +/- 0.07 and 0.62 +/- 0.07 ml/min respectively. During the second day after induction of ischaemic (glycerol and arterial clamping) acute tubular necrosis, rats with reduced plasma osmolality exhibited a similar worsening in CCR as on the first day, when compared with that in rats with normal osmolality. In rats with acute tubular necrosis induced with mercuric chloride reduction in plasma osmolality did not aggravate the severity of renal failure. These results show that acute fall in plasma osmolality worsens the renal failure in the ischaemic but not in the nephrotoxic models of acute tubular necrosis.

Acute Kidney Injury↗
PubMed1985

24,25(OH)2D3 enhances the calcemic effect of 1,25(OH)2D3.

The effect of 24,25(OH)2D3 on 1,25(OH)2D3-induced hypercalcemia was studied in normal rats. Serum (S) levels and urinary excretion of Ca2+ (UCaV) were measured in (a) control rats, (b) rats receiving a daily sc injection of 54 ng 1,25(OH)2D3, (c) rats receiving 24,25(OH)2D3 in the same dose and same manner, and (d) rats receiving 1,25(OH)2D3 + 24,25(OH)2D3. The animals were housed in metabolic cages and 24-hr urine specimens were collected. After 24 hr SCa2+ increased similarly with 1,25(OH)2D3 and with 1,25(OH)2D3 + 24,25(OH)2D3, while 24,25(OH)2D3 alone did not change SCa2+. UCaV after 24 hr increased significantly less (P less than 0.025) with 1,25(OH)2D3 + 24,25(OH)2D3 than with 1,25(OH)2D3 alone. After 5 days of 1,25(OH)2D3, SCa2+ rose from 5.1 +/- 0.15 to 6.29 +/- 0.08 whereas 1,25(OH)2D3 + 24,25(OH)2D3 effected a greater increase in SCa2+ up to 6.63 +/- 0.09 (P less than 0.01). 24,25(OH)2D3 alone did not change SCa2+. UCaV after 5 days of treatment rose similarly with 1,25(OH)2D3 and with 1,25(OH)2D3 + 24,25(OH)2D3. After 10 days of 1,25(OH)2D3 SCa2+ was 6.17 +/- 0.15 meq/liter while with the combination SCa2+ rose to 6.74 +/- 0.2 (P less than 0.025). 24,25(OH)2D3 alone did not change SCa2+. These results show that (a) 24,25(OH)2D3 alone does not alter SCa2+ in normal rats, (b) combined administration of 1,25(OH)2D3 + 24,25(OH)2D3 enhances the hypercalcemic response to 1,25(OH)2D3 without a parallel increase in UCaV, and (c) it is suggested that the effect of 24,25(OH)2D3 on serum Ca2+ level, at least partly, may result from its hypocalciuric effect.

24,25-Dihydroxyvitamin D 3↗
PubMed1985

Vitamin D-dependent rickets types I and II. Diagnosis and response to therapy.

The diagnostic value of measuring serum vitamin D metabolites is demonstrated in the present study in which two patients with vitamin D-dependent rickets (VDDR) Types I and II are reported. The patient with sporadic VDDR Type I was severely disabled and unable to walk. Her serum 1,25(OH)2D level was low (32 pg/ml, normal 30 to 60) and she responded dramatically to 1 microgram of 1 alpha-hydroxyvitamin D3 daily. The VDDR Type II patient had an autosomal recessive inheritance and total alopecia. His serum 1,25(OH)2D level was greater than 500 pg/ml, compatible with end-organ refractoriness to 1,25(OH)2D. He did not respond to daily doses of 1 microgram 1 alpha-hydroxyvitamin D3. These cases demonstrate the striking difference in 1,25(OH)2D levels and therapeutic response to 1,25(OH)2D in these two conditions.

Adult↗
PubMed1984

The effect of streptozotocin-induced diabetes mellitus on urinary excretion of sodium and renal Na+-K+-ATPase activity.

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 less than 0.001), 0.85 +/- 0.03 (P less than 0.001), 129.8 +/- 5.8 (P less than 0.001) and 129 +/- 5.8 (P less than 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 (mumoles Pi/mg prot/h) respectively. 24 h after DM induction Na-K-ATPase activity in the cortex rose to 59.3 +/- 2.4 (P less than 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 less than 0.001) after 3 days and remained high after 7 days. These findings show that streptozotocin-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.

Absorption↗
PubMed1984

Renal refractoriness to PTH in experimental Fanconi syndrome: evidence for intact adenylate cyclase activation.

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 (mean +/- SE) to 16.8 +/- 3.5 pmoles cAMP/mg prot/min (P less than 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 less than 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 less than 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 less than 0.001). For the difference in the increment between the control and FS group, P less than 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 less than 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.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine Triphosphate↗
PubMed1984

Effect of divalent ions on basal and hormone-activated renal adenylate cyclase/cyclic AMP system.

To elucidate the effect of Ca++ on adenylate cyclase (AC)/cyclic AMP system and its response to parathyroid hormone (PTH), experiments with parathyroidectomized rats' renal cortical tissue were performed in vitro. Increasing Ca++ from 0 to 5 mM reduced basal AC from 5.4 +/- (SE) 0.5 to 2.5 +/- 0.2 pmol cyclic AMP/mg protein/min (p less than 0.001). Raising Mg++ from 5 mM (basal concentration) to 20 mM restored AC to 5.7 +/- 0.55 (p less than 0.001). Adding 1 mM Mn++ to the incubation medium without Ca++ raised basal AC activity from 5.8 +/- 0.4 to 10.8 +/- 1.35 (p less than 0.01) and reversed the Ca++-induced inhibition. NaF-stimulated AC was reduced from 77.8 +/- 5.4 to 41.0 +/- 3.8 by 5 mM Ca++ (p less than 0.001), while adding Mg++ abolished this effect. PTH- and calcitonin-induced increase in AC was relatively resistant to Ca++ inhibition. Increasing Mn++ concentration from 0 to 5 mM (without Mg++) completely abolished PTH-induced increase in AC. The apparent Km of basal AC for Mg++ was 2.4, while in the presence of PTH the Km of AC for Mg++ was reduced to 1.1. The relative resistance of the PTH-induced increase in AC to Ca++ inhibition as opposed to the response of the basal activity to Ca++ may be explained by PTH-increased affinity of AC for Mg++.

Adenylyl Cyclases↗
PubMed1984

Ethnic differences in kidney graft survival.

Results of 73 first cadaveric donor renal transplants in Jerusalem between 1975 and 1980 are presented. There was a better 12-month graft survival in Arabs than in Jews (70.8% vs. 40.8%, P less than 0.035); however, 12-month patient survival was similar (83.3% vs. 85.7%). Acute rejection as the primary cause of graft loss occurred in 12.5% of the Arabs and 38.8% of the Jews (P less than 0.05). HLA-A, -B and -DR antigen-sharing was similar in both groups. Early acute rejection episodes had a poorer prognosis in Jews. Possible explanations for these findings are discussed, but the reason for the higher success rate in Arabs remains obscure.

Adolescent↗
PubMed1983

Sodium-dependent idiopathic hypercalciuria in renal-stone formers.

Four patients with renal stones had hypercalciuria which was dependent on a high sodium intake. Moderate sodium restriction corrected the hypercalciuria. Sodium excretion should be measured in all patients with idiopathic hypercalciuria so that the easily treated sodium-dependent hypercalciuria can be diagnosed.

Adult↗
PubMed1983

Blockade of the renal tubular effects of vitamin D by cycloheximide in the rat.

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 less than 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.

Adenylyl Cyclases↗
PubMed1983

Polyuria in experimental intrahepatic cholangitis induced by alpha-naphthyl-isothiocyanate.

Alpha-naphthyl-isothiocyanate (ANIT)-induced intrahepatic cholangitis was associated with significant polyuria in rats. The urine output in the experimental rats was about two and a half to four fold higher than that in the controls. The polyuria was accompanied by polydypsia and disappeared when water intake was limited and controlled. The glomerular filtration rate and renal histology remained intact. Dilution and concentration capacities were preserved and the response to exogenous anti-diuretic hormone was intact. Following water deprivation, the water and electrolyte contents of the renal medulla and papilla were similar in both experimental and control rats. The excretion of a salt-load in ANIT-treated rats was delayed. It is concluded that the polyuria in ANIT-treated rats is secondary to polydypsia. The finding of preserved dilution and concentration capacities in this experimental model contrasts to that in other experimental models of hepatobiliary disease.

1-Naphthylisothiocyanate↗
PubMed1983

Renal effect of vitamin D metabolites: evidence for the essential role of the 25(OH) group.

The effects of 1 alpha (OH)vitamin D3 [1 alpha (OH)D3] and 24,25(OH)2vitamin D3 [24,25(OH)2D3] on the phosphaturic action of parathyroid hormone (PTH) were studied in two groups of parathyroidectomized (PTX) rats. In group 1, PTX PTH-infused rats received intravenous 1 alpha (OH)D3, and in group 2, PTX PTH-infused rats received intravenous 24,25(OH)2D3. PTX PTH-infused rats served as controls. The effects of both vitamin D metabolites on renal PTH-activated adenylate cyclase (AC) were studied in vitro. In group 1, PTH increased fractional excretion of phosphate (CP/CIn) from 0.045 +/- 0.012 (+/- SE) to 0.263 +/- 0.011 (P less than 0.005). 1 alpha (OH)D3 failed to influence this response. In group 2, PTH increased CP/CIn from 0.055 +/- 0.008 to 0.289 +/- 0.027 (P less than 0.005). 24,25(OH)2D3 reduced the PTH-induced rise in CP/CIn from 0.289 +/- 0.027 to 0.192 +/- 0.021 (P less than 0.01) and decreased the urinary excretion of adenosine 3',5'-cyclic monophosphate. In vitro, 24,25(OH)2D3 blunted the PTH-activated AC, whereas 1 alpha (OH)D3 had no effect. These results show that 24,25(OH)D3, similar to two other 25(OH) metabolites of vitamin D-25(OH)vitamin D3 and 1,25(OH)2vitamin D3-suppresses the phosphaturic action of PTH, whereas 1 alpha(OH)D3, which is devoid of a 25(OH) group, lacks this effect. This suggests that a 25(OH) group is a prerequisite for the antiphosphaturic effect of vitamin D, whereas the 1 alpha (OH) group is not essential for this action.

24,25-Dihydroxyvitamin D 3↗
PubMed1983

Multiple myeloma presenting as dense deposit disease. Light chain nephropathy.

A 45-year-old male was admitted to the hospital because of polyuria and polydipsia. After admission, proteinuria and hematuria were found. The kidney function deteriorated and necessitated the initiation of chronic hemodialysis. Examination of the bone marrow revealed multiple myeloma and kappa light chains were found in the urine. The kidney biopsy showed membranoproliferative glomerulonephritis with dense deposits in the glomerular basement membrane.

Basement Membrane↗