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    Wyświetlanie 1-6 z 6
    Tytuł:
    Time-dependent effect of leptin on renal Na+,K+-ATPase activity
    Autorzy:
    Marciniak, Andrzej
    Jamroz-Wiśniewska, Anna
    Borkowska, Ewelina
    Bełtowski, Jerzy
    Powiązania:
    https://bibliotekanauki.pl/articles/1041321.pdf
    Data publikacji:
    2005
    Wydawca:
    Polskie Towarzystwo Biochemiczne
    Tematy:
    mitogen-activated protein kinases
    leptin
    obesity
    arterial hypertension
    hydrogen peroxide
    Na+,K+-ATPase
    Opis:
    Leptin, secreted by adipose tissue, is involved in the pathogenesis of arterial hypertension, however, the mechanisms through which leptin increases blood pressure are incompletely elucidated. We investigated the effect of leptin, administered for different time periods, on renal Na+,K+-ATPase activity in the rat. Leptin was infused under anesthesia into the abdominal aorta proximally to the renal arteries for 0.5-3 h. Leptin administered at doses of 1 and 10 µg/min per kg for 30 min decreased the Na+,K+-ATPase activity in the renal medulla. This effect disappeared when the hormone was infused for ≥1 h. Leptin infused for 3 h increased the Na+,K+-ATPase activity in the renal cortex and medulla. The stimulatory effect was abolished by a specific inhibitor of Janus kinases (JAKs), tyrphostin AG490, as well as by an NAD(P)H oxidase inhibitor, apocynin. Leptin increased urinary excretion of hydrogen peroxide (H2O2) between 2 and 3 h of infusion. The effect of leptin on renal Na+,K+-ATPase and urinary H2O2 was augmented by a superoxide dismutase mimetic, tempol, and was abolished by catalase. In addition, infusion of H2O2 for 30 min increased the Na+,K+-ATPase activity. Inhibitors of extracellular signal regulated kinases (ERKs), PD98059 or U0126, prevented Na+,K+-ATPase stimulation by leptin and H2O2. These data indicate that leptin, by acting directly within the kidney, has a delayed stimulatory effect on Na+,K+-ATPase, mediated by JAKs, H2O2 and ERKs. This mechanism may contribute to the abnormal renal Na+ handling in diseases associated with chronic hyperleptinemia such as diabetes and obesity.
    Źródło:
    Acta Biochimica Polonica; 2005, 52, 4; 803-809
    0001-527X
    Pojawia się w:
    Acta Biochimica Polonica
    Dostawca treści:
    Biblioteka Nauki
    Artykuł
    Tytuł:
    Nitric oxide - superoxide cooperation in the regulation of renal Na+,K+-ATPase.
    Autorzy:
    Bełtowski, Jerzy
    Marciniak, Andrzej
    Jamroz-Wiśniewska, Anna
    Borkowska, Ewelina
    Powiązania:
    https://bibliotekanauki.pl/articles/1041505.pdf
    Data publikacji:
    2004
    Wydawca:
    Polskie Towarzystwo Biochemiczne
    Tematy:
    H+,K+-ATPase
    Sch 28080
    superoxide anion
    Na+,K+-ATPase
    nitric oxide
    oxidative stress
    Opis:
    The aim of this study was to investigate whether endogenous superoxide anion is involved in the regulation of renal Na+,K+-ATPase and ouabain-sensitive H+,K+-ATPase activities. The study was performed in male Wistar rats. Compounds modulating superoxide anion concentration were infused under general anaesthesia into the abdominal aorta proximally to the renal arteries. The activity of ATPases was assayed in isolated microsomal fraction. We found that infusion of a superoxide anion-generating mixture, xanthine oxidase (1 mU/min per kg) + hypoxanthine (0.2 μmol/min per kg), increased the medullary Na+,K+-ATPase activity by 49.5% but had no effect on cortical Na+,K+-ATPase and either cortical or medullary ouabain-sensitive H+,K+-ATPase. This effect was reproduced by elevating endogenous superoxide anion with a superoxide dismutase inhibitor, diethylthiocarbamate. In contrast, a superoxide dismutase mimetic, TEMPOL, decreased the medullary Na+,K+-ATPase activity. The inhibitory effect of TEMPOL was abolished by inhibitors of nitric oxide synthase (L-NAME), soluble guanylate cyclase (ODQ) and protein kinase G (KT5823). The stimulatory effect of diethylthiocarbamate was not observed in animals pretreated with a synthetic cGMP analogue, 8-bromo-cGMP. An inhibitor of NAD(P)H oxidase, apocynin (1 μmol/min per kg), decreased the Na+,K+-ATPase activity in the renal medulla and its effect was prevented by L-NAME, ODQ or KT5823. In contrast, a xanthine oxidase inhibitor, oxypurinol, administered at the same dose was without effect. These data suggest that NAD(P)H oxidase-derived superoxide anion increases Na+,K+-ATPase activity in the renal medulla by reducing the availability of NO. Excessive intrarenal generation of superoxide anion may upregulate medullary Na+,K+-ATPase leading to sodium retention and blood pressure elevation.
    Źródło:
    Acta Biochimica Polonica; 2004, 51, 4; 933-942
    0001-527X
    Pojawia się w:
    Acta Biochimica Polonica
    Dostawca treści:
    Biblioteka Nauki
    Artykuł
    Tytuł:
    Spectrophotometric assay of renal ouabain-resistant Na+-ATPase and its regulation by leptin and dietary-induced obesity.
    Autorzy:
    Bełtowski, Jerzy
    Jamroz-Wiśniewska, Anna
    Nazar, Jarosław
    Wójcicka, Grażyna
    Powiązania:
    https://bibliotekanauki.pl/articles/1041514.pdf
    Data publikacji:
    2004
    Wydawca:
    Polskie Towarzystwo Biochemiczne
    Tematy:
    leptin
    obesity
    Na+,K+-ATPase
    Na+-ATPase
    Opis:
    Apart from Na+,K+-ATPase, a second sodium pump, Na+-stimulated, K+-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 μmol 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.
    Źródło:
    Acta Biochimica Polonica; 2004, 51, 4; 1003-1014
    0001-527X
    Pojawia się w:
    Acta Biochimica Polonica
    Dostawca treści:
    Biblioteka Nauki
    Artykuł
    Tytuł:
    Neuropathic pain and chronic pain as an underestimated interdisciplinary problem
    Autorzy:
    Szewczyk, Anna K.
    Jamroz-Wiśniewska, Anna
    Haratym, Natalia
    Rejdak, Konrad
    Powiązania:
    https://bibliotekanauki.pl/articles/2084915.pdf
    Data publikacji:
    2022-06-08
    Wydawca:
    Instytut Medycyny Pracy im. prof. dra Jerzego Nofera w Łodzi
    Tematy:
    treatment
    epidemiology
    chronic pain
    neuropathic pain
    occupational disorders
    musculoskeletal pain
    Opis:
    Neuropathic pain and chronic pain constitute an interdisciplinary problem on the border of medicine, psychology, sociology and economics. While it seems to be underestimated, the scale of this problem will continue to increase due to the population aging and the growing incidence of lifestyle disorders. People employed in various occupational sectors may also wrestle with these disease units, which affect the quality of their life, mental health and work productivity. A narrative review provided an overview of neuropathic pain and chronic pain, and their relationship to such factors as job type, work absenteeism and productivity decline, as well mental well-being. A systematic literature search was conducted based on the Preferred Reporting Items for Systematic Reviews and Meta-Analysis (PRISMA) guidelines to identify appropriate literature by searching the electronic databases: PubMed/MEDLINE, Pain Journal and the Cochrane Database of Systematic Reviews. Studies were published in Polish, English and French. Research shows an increasing number of musculoskeletal diseases in professionally active people, which lead to disability or provoke work absences. However, sickness presenteeism and/or absenteeism caused by pain not only leads to economic burdens, but also to burnout, fatigue and depression syndromes in employees. These disorders may require specialized effective interventions to support the return to work or maintaining employment despite experiencing pain. Every patient with chronic or neuropathic pain should be correctly assessed to determine the best method of treatment and its effectiveness.
    Źródło:
    International Journal of Occupational Medicine and Environmental Health; 2022, 35, 3; 249-264
    1232-1087
    1896-494X
    Pojawia się w:
    International Journal of Occupational Medicine and Environmental Health
    Dostawca treści:
    Biblioteka Nauki
    Artykuł
    Tytuł:
    Bidirectional regulation of renal cortical Na+,K+-ATPase by protein kinase C.
    Autorzy:
    Bełtowski, Jerzy
    Marciniak, Andrzej
    Jamroz-Wiśniewska, Anna
    Borkowska, Ewelina
    Wójcicka, Grażyna
    Powiązania:
    https://bibliotekanauki.pl/articles/1041555.pdf
    Data publikacji:
    2004
    Wydawca:
    Polskie Towarzystwo Biochemiczne
    Tematy:
    phosphatidylinositol-3-kinase
    protein kinase C
    cytochrome P450-dependent arachidonate metabolites
    Na+,K+-ATPase
    Opis:
    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 (10-11 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 Ki for ouabain. The effects of PDBu were abolished by PKC inhibitors, staurosporine, GF109203X, and Gö 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.
    Źródło:
    Acta Biochimica Polonica; 2004, 51, 3; 757-772
    0001-527X
    Pojawia się w:
    Acta Biochimica Polonica
    Dostawca treści:
    Biblioteka Nauki
    Artykuł
    Tytuł:
    Progressive forms of multiple sclerosis: disease-modifying therapy review
    Autorzy:
    Sapko, Klaudia
    Szczepańska-Szerej, Anna
    Jamroz-Wiśniewska, Anna
    Kulczyński, Marcin
    Marciniec, Michał
    Rejdak, Konrad
    Powiązania:
    https://bibliotekanauki.pl/articles/1167060.pdf
    Data publikacji:
    2018
    Wydawca:
    Przedsiębiorstwo Wydawnictw Naukowych Darwin / Scientific Publishing House DARWIN
    Tematy:
    Disease-modifying drugs
    Multiple sclerosis
    New therapy
    Primary-progressive MS
    Secondary-progressive MS
    Opis:
    Multiple sclerosis (MS) is a demyelinating, inflammatory, autoimmune disease of the central nervous system which affects most commonly young adults. It has wide spectrum of clinical and radiological presentations with relapses or steady progression. Recent years have brought new reports on the pathogenesis of MS. This systematized the current MS classification and created new parameters describing the course of the disease, such as activity and progression. Attention has been paid to the need for new drugs that focus on the treatment of progressive MS. Until now, the primary and secondary progressive MS have been somewhat forgotten, and most of modifying-disease drugs have been registered in the treatment of relapsing-remitting subtype. In recent years, not only new drug has been registered for the treatment of progressive MS (ocrelizumab) and another one is planned to be approved soon (siponimod), but also indications of old medicines (interferon-beta1b, cladribine, mitoxantrone, cyclophosphamide, azathioprine) have been extended. Despite intensive development, there is still a great need to seek new drugs that will stop the progression of disability in MS patients.
    Źródło:
    World Scientific News; 2018, 105; 157-167
    2392-2192
    Pojawia się w:
    World Scientific News
    Dostawca treści:
    Biblioteka Nauki
    Artykuł
      Wyświetlanie 1-6 z 6

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