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1

Informacje na temat projektów badawczych, zakwalifikowanych przez Komitet Badań Naukowych do dofinansowania w XIV konkursie (granty)

100%
Wojcicka G.
Człowiek i Środowisko
|
1998
|
tom 22
|
nr 4
2

Informacje na temat projektów badawczych zakwalifikowanych przez Komitet Badań Naukowych do dofinansowania z budżetu państwa (granty)

100%
Wojcicka G.
Człowiek i Środowisko
|
1998
|
tom 22
|
nr 1-2
3

Lokalny rynek nieruchomosci na obszarach o szczegolnie wysokich walorach naturalnych i kulturowych na przykladzie gminy Konstancin

100%
Wojcicka G.
Człowiek i Środowisko
|
1999
|
tom 23
|
nr 4
409-422
W ramach prac badawczych, realizowanych z działalności statutowej Instytutu, jako Problem Badawczy nr 6 pt. „Poszukiwanie modelu teoretycznego dla aktywnie funkcjonującego rynku nieruchomości w gminie opracowano m.in. „Rynek nieruchomości na obszarach o szczególnie wysokich walorach naturalnych i kulturowych na przykładzie uzdrowiska Konstancin". Analiza rynku nieruchomości została wstępnie opracowana (I etap) na podstawie informacji o cenach transakcyjnych z lat 1997- 1998 (informacje zaczerpnięto z aktów notarialnych). W latach tych odnotowano jedynie 74 transakcje kupna-sprzedaży, a dotyczyły one: 24 działek rolnych, 32 działek budowlanych niezabudowanych, 15 działek budowlanych zabudowanych, 3 mieszkań w zabudowie blokowej (parter - z przeznaczeniem na otworzenie banku). Przy wykorzystaniu technik komputerowych, naniesiono na mapę w skali 1:10 000, informacje w postaci warstw: 1/ mapa średnich cen gruntów (wg stanu na 1997r.) - opracowanie geodezyjne Urzędu Wojewódzkiego w Warszawie, Wydział Geodezji, Kartografii, Katastru i Gospodarki Gruntami, 2/ strefy ochrony uzdrowiskowej, 3/ walory przyrodnicze (rezerwaty, parki krajobrazowe i lasy), 4/ zabytki (zabytkowe wille i pensjonaty), 5/ infrastrukturę uzdrowiskową (punkty lecznictwa otwartego, tężnia i park zdrojowy), 6/ uzbrojenie terenu (linie energetyczne, tereny zwodociągowane i tereny zgazyfikowane, studnie kopane, linia telefoniczna), oraz 7/ drogi o znaczeniu wojewódzkim i lokalnym. W wyniku nałożenia kilkunastu warstw informacyjnych dokonana została ocena rozkładu czynników decydujących o cenach nieruchomości. Przyjęta została teza, że na poziom cen na lokalnym rynku nieruchomości istotny wpływ mają rynkowe cechy nieruchomości: położenie w strefie A, B i C ochrony uzdrowiskowej, sąsiedztwo zabytków, uzbrojenie (gazociąg, wodociąg, elektryczność), dostępność komunikacyjna. Wnioski ukierunkowano na wyróżnienie cech i walorów środowiska przyrodniczego i kulturowego, które mogą mieć istotny wpływ na wartości rynkowe nieruchomości. Cechom rynkowym na wytypowanych obszarach nadane zostały odpowiednie wagi (obliczone i ujęte w tabele i przedstawione na schematach). Przeprowadzona analiza potwierdza hipotezę, że atrakcyjność rynku nieruchomości wynika z obecności licznych zabytków architektury wkomponowanych w zaciszne otoczenie, co z kolei ma związek z dobrym zagospodarowaniem przestrzennym obszaru, będącym konsekwencją wieloletniej tradycji szczególnych zasad ochrony. Liczy się też uzbrojenie terenu w media oraz dogodne położenie w stosunku do tras komunikacyjnych, ułatwiających dostęp do ośrodków lecznictwa i rehabilitacji. Teren uzdrowiska stanowi więc korzystne miejsce inwestowania tych, którzy cenią sobie ciszę, spokój oraz piękno przyrody i gwarancję „zdrowego klimatu". Z przeprowadzonej analizy wynika, że wraz ze wzrostem poziomu świadomości ekologicznej społeczeństwa, rosną wymagania dotyczące stanu środowiska przyrodniczego i ochrony dziedzictwa kulturowego. Tendencje te potwierdzają różnice w cenach nieruchomości w poszczególnych strefach ochrony uzdrowiskowej. Ma to związek z dobrym zagospodarowaniem przestrzeni i konsekwencjami wieloletniej tradycji szczególnych zasad ochrony. Atrakcyjność rynku nieruchomości związana jest przede wszystkim z funkcją uzdrowiskową miejscowości o wieloletnich trądycjach i kulturowych, a wysokie walory środowiska przyrodniczego, podlegające szczególnym zasadom ochrony, są gwarantowane przepisami prawnymi w chwili obecnej i w przyszłości.
4

Wyniki prac badawczych realizowanych w ramach działalności statutowej Instytutu w 1998 roku

100%
Wojcicka G.
Człowiek i Środowisko
|
1999
|
tom 23
|
nr 2-3
5

Projekty badawcze zakwalifikowane przez Komitet Badań Naukowych do dofinansowania z budżetu państwa (granty)

100%
Wojcicka G.
Człowiek i Środowisko
|
2000
|
tom 24
|
nr 2
6

Decyzje KBN w sprawie dofinansowania prac naukowo-badawczych.

75%
Wojcicka G.
Człowiek i Środowisko
|
1998
|
tom 22
|
nr 3
293-296
7

Stres oksydacyjny w zapaleniu klebuszkow nerkowych

63%
Wojcicka G., Beltowski J.
Postępy Higieny i Medycyny Doświadczalnej
|
2001
|
tom 55
|
nr 6
855-869
8

Spectrophotometric method for the determination of renal ouabain-sensitive Hplus, Kplus-ATPase activity

63%
Beltowski J., Wojcicka G.
Acta Biochimica Polonica
|
2002
|
tom 49
|
nr 2
The aim of this work was to develop a method for renal H+,K+-ATPase measurement based on the previously used Na+ ,K+ -ATPase assay (Bełtowski et al.: J Physiol Pharmacol.; 1998, 49: 625-37). ATPase activity was assessed by measuring the amount of inorganic phosphate liberated from ATP by isolated microsomal fraction. Both ouabain-sensitive and ouabain-resistant K+ -stimulated and Na+ -independent ATPase activity was detected in the renal cortex and medulla. These activities were blocked by 0.2 mM imidazolpyridine derivative, Sch 28080. The method for ouabain- sensitive H+ ,K -ATPase assay is characterized by good reproducibility, linearity and recovery. In contrast, the assay for ouabain-resistant H ,K -ATPase was unsatisfac­tory, probably due to low activity of this enzyme. Ouabain-sensitive H+ ,K+ -ATPase was stimulated by K + with Km of 0.26 ± 0.04 mM and 0.69 ±0.11 mM in cortex and me­dulla, respectively, and was inhibited by ouabain (Ki of 2.9 ± 0.3 uM in the renal cortex and 1.9 ± 0.4 uM in the renal medulla) and by Sch 28080 (Ki of 1.8 ± 0.5 uM and 2.5 ± 0.9 uM in cortex and medulla, respectively). We found that ouabain-sensitive H+ ,K+ -ATPase accounted for about 12% of total ouabain-sensitive activity in the Na+ ,K+-ATPase assay. Therefore, we suggest to use Sch 28080 during Na+,K+-ATPase measurement to block H+ ,K+ -ATPase and improve the assay specificity. Leptin ad­ministered intraperitoneally (1 mg/kg) decreased renal medullary Na+ ,K+ -ATPase ac­tivity by 32.1% at 1 h after injection but had no effect on H+ ,K+ -ATPase activity sug­gesting that the two renal ouabain-sensitive ATPases are separately regulated.
9

Receptory aktywowane przez czynniki powodujace proliferacje peroksysomow [PPAR] w patofizjologii ukladu krazenia oraz perspektywy zastosowania agonistow tych receptorow w terapii

51%
Beltowski J., Wojcicka G., Jamroz A.
Postępy Higieny i Medycyny Doświadczalnej
|
2003
|
tom 57
|
nr 2
199-217
10

Sectrophotometric assay of renal ouabain-resistant Naplus-ATPase and its regulation by leptin and dietary-induced obesity

51%
Beltowski J., Jamroz-Wisniewska A., Nazar J., Wojcicka G.
Acta Biochimica Polonica
|
2004
|
tom 51
|
nr 4
Apart from Na,K-ATPase, a second sodium pump, Na-stimulated, ^-independ­ent ATPase (Na -ATPase) is expressed in proximal convoluted tubule of the mamma­lian kidney. The aim of this study was to develop a method of Na -ATPase assay based on the method previously used by us to measure Na ,K -ATPase activity (Acta Biochim Polon.; 2002, 49: 515-27). The ATPase activity was assayed as the amount of inorganic phosphate liberated from ATP by isolated microsomal fraction. Na -ATPase activity was calculated as the difference between the activities mea­sured in the presence and in the absence of 50 mM NaCl. Na -ATPase activity was detected in the renal cortex (3.5 ± 0.2 ^mol phosphate/h per mg protein), but not in the renal medulla. Na -ATPase was not inhibited by ouabain or an H ,K -ATPase in­hibitor, Sch 28080, but was almost completely blocked by 2 mM furosemide. Leptin administered intraperitoneally (1 mg/kg) decreased the Na ,K -ATPase activity in the renal medulla at 0.5 and 1 h by 22.1% and 27.1%, respectively, but had no effect on Na -ATPase in the renal cortex. Chronic hyperleptinemia induced by repeated subcutaneous leptin injections (0.25 mg/kg twice daily for 7 days) increased cortical Na,K-ATPase, medullary Na,K-ATPase and cortical Na+-ATPase by 32.4%, 84.2% and 62.9%, respectively. In rats with dietary-induced obesity, the Na ,K - ATPase activity was higher in the renal cortex and medulla by 19.7% and 34.3%, re­spectively, but Na -ATPase was not different from control. These data indicate that both renal Na -dependent ATPases are separately regulated and that up-regulation of Na -ATPase may contribute to Na retention and arterial hypertension induced by chronic hyperleptinemia.
11

Species- and substrate-specific stimulation of human plasma paraoxonase 1 [PON1] activity by high chloride concentration

51%
Beltowski J., Wojcicka G., Marciniak A.
Acta Biochimica Polonica
|
2002
|
tom 49
|
nr 4
Paraoxonase 1 (PON1), contained in plasma high-density lipoproteins, plays an im­portant role in the protection of plasma lipoproteins and cell membranes from oxida­tive damage. Previous studies indicate that human PON1 is stimulated by high NaCl concentrations. The aim of this study was to characterize in more detail the effect of salts on serum PON1. Paraoxon-hydrolyzing activity of human serum was stimulated by 81.6% following the addition of 1 M NaCl. The effect of NaCl was dose-dependent between 0.5 and 2 M. PON1 activity toward phenyl acetate was reduced by 1 M NaCl by 55.2%. Both the paraoxon- and phenyl acetate-hydrolysing activity was slightly lower in heparinized plasma than in serum, but NaCl had similar stimulatory and in­hibitory effects on these activities, respectively. In rat, rabbit, and mouse, NaCl re­duced PON1 activity. KCl had a similar effect on human PON1 as NaCl. Sodium nitrite also stimulated human PON1 but much less effectively than chloride salts. In contrast, sucrose, sodium acetate and sodium lactate had no significant effect. NaBr was a less effective PON1 activator than NaCl, whereas the effect of NaJ was non-significant. The activity of human PON1 toward homogentisic acid lactone and y-decanolactone was unaltered by NaCl. These data indicate that: 1) high concentrations of chlorides stimulate human PON1 activity toward paraoxon but not other substrates, 2) PON1 is inhibited by Cl- in other mammalian species, 3) the potency of human PON1 activa­tion by halogene salts increases with decreasing atomic mass of the halide anion.
12
Content available remote

Leptin decreases renal medullary Na plus, K plus-ATPase activity through phosphatidylinositol 3-kinase dependent mechanism

51%
Beltowski J., Marciniak A., Wojcicka G.
Journal of Physiology and Pharmacology
|
2004
|
tom 55
|
nr 2
We examined the effect of leptin on renal function and renal Na+,K+-ATPase and ouabain-sensitive H+,K+-ATPase activities in the rat. Leptin was infused under general anaesthesia into the abdominal aorta proximally to the renal arteries. Leptin infused at doses of 1 and 10 µg/kg/min increased urine output by 40% and 140%, respectively. Urinary Na+ excretion increased in rats receiving leptin at doses of 0.1, 1, and 10 µg/kg/min by 57.6%, 124.2% and 163.6%, respectively. Leptin had no effect on creatinine clearance, potassium excretion and phosphate excretion. Na+,K+-ATPase activity in the renal medulla of rats treated with 1 and 10 µg/kg/min leptin was lower than in control animals by 25.5% and 33.2%, respectively. In contrast, cortical Na+,K+-ATPase as well as either cortical or medullary ouabain-sensitive H+,K+-ATPase activities did not differ between leptin-treated and control animals. The effect of leptin on Na+,K+-ATPase activity was abolished by actin depolymerizing agents, cytochalazin D and latrunculin B, and by phosphatidylinositol 3-kinase (PI3K) inhibitors, wortmannin and LY294002. These results indicate that: 1) natriuretic effect of leptin is mediated, at least in part, by decrease in renal medullary Na+,K+-ATPase activity, 2) inhibition of medullary Na+,K+-ATPase by leptin is mediated by PI3K and requires integrity of actin cytoskeleton.
13

Regulation of renal NAplus, Kplus-ATPase and ouabain-sensitive Hplus, Kplus-ATPase by the cyclic AMP-protein kinase A signal transduction pathway

51%
Beltowski A., Marciniak A., Wojcicka G., Gorny D.
Acta Biochimica Polonica
|
2003
|
tom 50
|
nr 1
We investigated the effect of the cyclic AMP-protein kinase A (PKA) signalling path­way on renal Na+ ,K+ -ATPase and ouabain-sensitive H+ ,K+ -ATPase. Male Wistar rats were anaesthetized and catheter was inserted through the femoral artery into the ab­dominal aorta proximally to the renal arteries for infusion of the investigated sub­stances. Na+ ,K+ -ATPase activity was measured in the presence of Sch 28080 to block ouabain-sensitive H+ ,K+ -ATPase and improve specificity of the assay. Dibutyryl-cyclic AMP (db-cAMP) administered at a dose of 10-7 mol/kg per min and 10 -6mol/kg per min increased Na+ ,K+ -ATPase activity in the renal cortex by 34% and 42%, respec­tively, and decreased it in the renal medulla by 30% and 44%, respectively. db-cAMP infused at 10- mol/kg per min increased the activity of cortical ouabain-sensitive H+,K+ -ATPase by 33%, and medullary ouabain-sensitive H+,K+ -ATPase by 30%. All the effects of db-cAMP were abolished by a specific inhibitor of protein kinase A, KT 5720. The stimulatory effect on ouabain-sensitive H+ ,K+ -ATPase and on cortical Na+ ,K+ -ATPase was also abolished by brefeldin A which inhibits the insertion of pro­teins into the plasma membranes, whereas the inhibitory effect on medullary Na+ ,K+ -ATPase was partially attenuated by 17-octadecynoic acid, an inhibitor of cytochrome P450-dependent arachidonate metabolism. We conclude that the cAMP-PKA pathway stimulates Na+ ,K+ -ATPase in the renal cortex as well as ouabain-sensitive H+ ,K+ -ATPase in the cortex and medulla by a mechanism requiring insertion of proteins into the plasma membrane. In contrast, medullary Na+ ,K+ -ATPase is inhibited by cAMP through a mechanism involving cytochrome P450-dependent arachidonate metabolites.
14
Content available remote

Nitric oxide decreases renal medullary Naplus, Kplus-ATPase activity through cyclic GMP-protein kinase G dependent mechanism

51%
Beltowski J., Marciniak A., Wojcicka G., Gorny D.
Journal of Physiology and Pharmacology
|
2003
|
tom 54
|
nr 2
The aim of this study was to investigate the effect of nitric oxide on renal Na+,K+-ATPase and ouabain-sensitive H+,K+-ATPase activities. The study was performed in male Wistar rats. The investigated substances were infused under general anaesthesia into abdominal aorta proximally to the renal arteries. The activity of ATPases was assayed in isolated microsomal fraction. NO donor, S-nitroso-N-acetylpenicillamine (SNAP), infused at doses of 10-7 and 10-6 mol/kg/min decreased medullary Na+,K+-ATPase activity by 29.4% and 45.2%, respectively. Another NO donor, spermine NONOate, administered at the same doses reduced Na+,K+-ATPase activity in the renal medulla by 31.7% and 46.5%, respectively. Neither of NO releasers had any effect on Na+,K+-ATPase in the renal cortex and on either cortical or medullary ouabain-sensitive H+,K+-ATPase. Infusion of NO precursor, L-arginine (100 µmol/kg/min), decreased medullary Na+,K+-ATPase activity by 32.2%, whereas inhibitor of nitric oxide synthase, L-NAME (10 nmol/kg/min), increased this activity by 20.7%. The effect of synthetic NO donors was mimicked by 8-bromo-cGMP and blocked by inhibitors of soluble guanylate cyclase, ODQ or methylene blue, as well as by specific inhibitor of protein kinase G, KT5823. In addition, inhibitory effect of either SNAP or 8-bromo-cGMP on medullary Na+,K+-ATPase was abolished by 17-octadecynoic acid (17-ODYA), which inhibits cytochrome P450-dependent metabolism of arachidonic acid. These data suggest that NO decreases Na+,K+-ATPase activity in the renal medulla through the mechanism involving cGMP, protein kinase G, and cytochrome P450-dependent arachidonate metabolites. In contrast, NO has no effect on Na+,K+-ATPase in the renal cortex and on either cortical or medullary ouabain-sensitive H+,K+-ATPase.
15
Content available remote

The opposite effects of cyclic AMP-protein kinase a signal transduction pathway on renal cortical and medullary Naplus, Kplus-ATPase activity

51%
Beltowski J., Marciniak A., Wojcicka G., Gorny D.
Journal of Physiology and Pharmacology
|
2002
|
tom 53
|
nr 2
Cyclic AMP-protein kinase A (PKA) pathway plays an important role in signal transduction in renal tubular cells, however, its role in transport regulation is not completely established. The aim of this study was to investigate in vivo the effect of PKA on renal Na+, K+-ATPase activity. The study was performed in male Wistar rats. The animals were anaesthetized with pentobarbital and investigated drugs were infused through the catheter inserted into the abdominal aorta. Na+,K+-ATPase activity was assayed in an isolated microsomal fraction of the renal cortex and medulla. Cell-permeable cAMP analogue, dibutyryl-cAMP (db-cAMP), dose-dependently stimulated Na+,K+-ATPase in the renal cortex and inhibited in the renal medulla. Maximal stimulation (+38.5%) and inhibition (-46.8%) were observed at a dose of 10-6 mol/kg/min. Measurement of Na+,K+-ATPase activity at different Na+ concentrations revealed that in the renal cortex db-cAMP increased Vmax of the enzyme without any effect on sodium affinity, whereas in the renal medulla decrease in Vmax was accompanied by decreased sodium affinity, evidenced by elevated K0.5 for sodium. The effect of db-cAMP was mimicked by the infusion of either adenylate cyclase activator, forskolin, or inhibitor of phosphodiesterase, IBMX. Both stimulatory and inhibitory effects of db-cAMP were prevented by pretreatment with protein kinase A inhibitor, KT 5720 (10-8 mol/kg/min) but not by inhibitor of protein kinase G, KT 5823. The inhibitory effect in the renal medulla was partially blocked by pretreatment with either ethoxyresorufin or 17-ODYA – two nonspecific inhibitors of cytochrome P450-dependent arachidonate metabolism, whereas an inhibitor of epoxygenase, miconazole, was not effective. Infusion of 20-hydroxyeicosatetraenoic acid (20-HETE) at a dose of 10-10 mol/kg/min decreased medullary Na+,K+-ATPase activity by 24.2%. Exogenous protein phosphatases inhibitor, okadaic acid (OA, 10-8-10-7 mol/kg/min) caused dose-dependent decrease in renal medullary Na+,K+-ATPase activity, maximally by 31.9%, but had no effect in the renal cortex. The effects of OA and db-cAMP in the renal medulla were not additive. When OA administration (10-7 mol/kg/min) was followed by 20-HETE (10-10 mol/kg/min), medullary Na+,K+-ATPase activity decreased by 48.6% and was similar as after db-cAMP. We conclude, that cAMP-PKA pathway activates Na+,K+-ATPase in the renal cortex and inhibits in the renal medulla. The inhibitory effect is partially mediated by cytochrome P450-dependent arachidonate metabolites and possibly also by PKA-dependent inhibition of protein phosphatases.
16
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Content available

The effect of dietary-induced obesity on lipid peroxidation, antioxidant enzymes and total plasma antioxidant capacity

51%
Beltowski J., Wojcicka G., Gorny D., Marciniak A.
Journal of Physiology and Pharmacology
|
2000
|
tom 51
|
nr 4,2
17
Content available remote

The effect of peroxisome proliferator-activated receptors alpha (PPARalpha) agonist, fenofibrate, on lipid peroxidation, total antioxidant capacity, and plasma paraoxonase 1 (PON1) activity

51%
Beltowski J., Wojcicka G., Mydlarczyk M., Jamroz A.
Journal of Physiology and Pharmacology
|
2002
|
tom 53
|
nr 3
The aim of this study was to investigate the effect of peroxisome proliferator activated receptors alpha agonist, fenofibrate, on the level of oxidative stress, total antioxidant capacity, and plasma paraoxonase 1 (PON1) activity in the rat. The adult male Wistar rats received fenofibrate for 7 days. The drug was added to food at concentrations 0.005%, 0.05% and 0.5%, which corresponded to doses of 3, 30 and 300 mg/kg/day, respectively. Fenofibrate treatment dose-dependently reduced plasma concentration of malonyldialdehyde and 4-hydroxydialkenals. The level of these lipid peroxidation products in animals treated with 0.005%, 0.05% and 0.5% fenofibrate was lower than in control group by 52.8%, 62.7% and 87.1%, respectively. Lipid hydroperoxides in plasma decreased by 29.7%, 23.4% and 27.5% in these groups, respectively. The drug had no significant effect on total antioxidant capacity measured as ferric reducing ability of plasma (FRAP). Paraoxon-hydrolyzing activity (PON) of plasma paraoxonase was 81.5% lower in animals receiving 0.05% fenofibrate and 69.2% lower in rats treated with 0.5% fenofibrate than in control. Phenyl acetate hydrolyzing activity (arylesterase, AE) was reduced by 15.2%, 49.6% and 55.8% in rats receiving 0.005%, 0.05% and 0.5% fenofibrate, respectively. PON/AE ratio decreased following 0.05% and 0.5% fenofibrate by 64.9% and 30.4%, respectively. The drug had no significant effect on total plasma triglycerides and cholesterol concentrations. The results indicate that fenofibrate treatment favourably modulates oxidant-antioxidant balance and unfavourably affects plasma PON1 activity in normolipidemic rats. These effects can contribute to the influence of PPARalpha agonists on pathological processes involved in atherogenesis.
18

Bidirectional regulation of renal cortical Naplus, Kplus-ATPase by protein kinase C

45%
Beltowski J., Marciniak A., Jamroz-Wisniewska A., Borkowska E., Wojcicka G.
Acta Biochimica Polonica
|
2004
|
tom 51
|
nr 3
We examined the role of protein kinase C (PKC) in the regulation of Na+,K+- ATPase activity in the renal cortex. Male Wistar rats were anaesthetized and the in­vestigated reagents were infused into the abdominal aorta proximally to the renal ar­teries. A PKC-activating phorbol ester, phorbol 12,13-dibutyrate (PDBu), had a dose-dependent effect on cortical Na+ ,K+ -ATPase activity. Low dose of PDBu (10- mol/kg per min) increased cortical Na+ ,K+ -ATPase activity by 34.2%, whereas high doses (10-9 and 10-8 mol/kg per min) reduced this activity by 22.7% and 35.0%, respectively. PDBu administration caused changes in Na+ ,K+ -ATPase Vmax without af­fecting K0.5 for Na+ , K+ and ATP as well as K for ouabain. The effects of PDBu were abolished by PKC inhibitors, staurosporine, GF109203X, and Go 6976. The inhibi­tory effect of PDBu was reversed by pretreatment with inhibitors of cytochrome P450-dependent arachidonate metabolism, ethoxyresorufin and 17-octadecynoic acid, inhibitors of phosphatidylinositol 3-kinase (PI3K), wortmannin and LY294002, and by actin depolymerizing agents, cytochalasin D and latrunculin B. These results suggest that PKC may either stimulate or inhibit renal cortical Na+ ,K+ -ATPase. The inhibitory effect is mediated by cytochrome P450-dependent arachidonate metabo­lites and PI3K, and is caused by redistribution of the sodium pump from the plasma membrane to the inactive intracellular pool.
19
Content available remote

Protective effects of melatonin against thioacetamide-induced liver fibrosis in rats

39%
Czechowska G., Celinski K., Korolczuk A., Wojcicka G., Dudka J., Bojarska A., Reiter R. J.
Journal of Physiology and Pharmacology
|
2015
|
tom 66
|
nr 4
20
Content available remote

The effect of the angiotensin II receptor, type 1 receptor antagonists, losartan and telmisartan, on thioacetamide-induced liver fibrosis in rats

33%
Czechowska G., Celinski K., Korolczuk A., Wojcicka G., Dudka J., Bojarska A., Madro A., Brzozowski T.
Journal of Physiology and Pharmacology
|
2016
|
tom 67
|
nr 4
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