Wyniki wyszukiwania

1

Variation of the structure and course of the interlobular arteries in human kidney

100%

Kosinski H.

Folia Morphologica

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1997

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tom 56

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nr 4

2

Variation of the structure and course of the interlobular arteries in human kidney

100%

Kosinski H.

Folia Morphologica

|

1996

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tom 55

|

nr 4

3

TGF-beta1 immunohistochemistry and promoter methylation in chronic renal failure rats treated with uremic clearance granules

84%

Miao X.-H., Wang C.-G., Hu B.-Q., Li A., Chen C.-B., Song W.-Q.

Folia Histochemica et Cytobiologica

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2010

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tom 48

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nr 2

284-291

4

Renal tissue NO and intrarenal haemodynamics during experimental variations of NO content in anaesthetised rats

84%

Grzelec-Mojzesowicz M., Sadowski J.

Journal of Physiology and Pharmacology

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2007

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tom 58

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nr 1

Direct renal nitric oxide (NO) measurements were infrequent and no simultaneous measurements of renal cortical and medullary NO and local perfusion were reported. Large-surface NO electrodes were placed in renal cortex and medulla of anaesthetised rats; simultaneously, renal blood flow (RBF, index of cortical perfusion) and medullary laser-Doppler flux (MBF) were determined. NO synthase inhibitors: nonselective (L-NAME) or selective for neuronal NOS (nNOS) (S-methyl-thiocitrulline, SMTC), and NO donor (SNAP), were used to manipulate tissue NO. Baseline tissue NO was significantly higher in medulla (703±49 nM) than in cortex (231±17 nM). Minimal cortical and medullary NO current measured after maximal L-NAME dose (2.4 mg kg-1 i.v.) was taken as tissue NO zero level. This dose decreased RBF and MBF significantly (-43%). SMTC, 1.2 mg kg-1 h-1 i.v., significantly decreased tissue NO by 105±32 nM in cortex and 546±64 nM in medulla, RBF and MBF decreased 30% and 20%, respectively. Renal artery infusion of SNAP, 0.24 mg kg-1 min-1 significantly increased tissue NO by 139±18 nM in cortex and 948±110 nM in medulla. Since inhibition of nNOS decreased medullary NO by 80% and MBF by 20% only, this isoform has probably minor role in the maintenance of medullary perfusion.

5

The effects of indomethacin on angiogenic factors mRNA expression in renal cortex of healthy rats

84%

Mucha K., Foroncewicz B., Koziak K., Czarkowska-Paczek B., Paczek L.

Journal of Physiology and Pharmacology

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2007

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tom 58

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nr 1

Indomethacin is a nonsteroidal anti-inflammatory drug used frequently to control chronic or temporary pain. In the kidney, indomethacin decreases medullary and cortical perfusion, resulting in hypoxia. Kidney hypoxia has many effects, including changes in gene expression, and is a strong stimulus for angiogenesis. Other angiogenic factors include vascular endothelial growth factor (VEGF), basic fibroblast growth factor (FGF-2), transforming growth factor beta 1 (TGFß1), and platelet-derived growth factor (PDGF). Our goal was to examine the influence of indomethacin on mRNA expression of these factors and their selected receptors in the renal cortex of healthy rats. Groups of 8 healthy, male, six-week-old Wistar rats received either indomethacin (5 mg/kg/day) or placebo orally for three months. RNA from renal cortex biopsies was analyzed by real-time polymerase chain reaction to quantify the mRNA levels of each cytokine. We observed significantly higher mRNA levels for VEGF (1.73-fold), FGF-2 (5.6-fold) and TGFß receptor III (2.93-fold), PDGF receptor alpha (2.93-fold) and receptor ß (2.91-fold) in rats receiving indomethacin compared to rats given placebo (p < 0.05). Amounts of mRNA for TGFß1, PDGF, FGF receptors 1 and 2 and TGFß receptor I did not differ between analysed groups. Our data indicates that indomethacin may regulate the expression of potent angiogenic factors VEGF and FGF-2.

6

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

84%

Beltowski J., Marciniak A., Jamroz-Wisniewska A., Borkowska E., Wojcicka G.

Acta Biochimica Polonica

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2004

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tom 51

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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.

7

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

84%

Beltowski J., Marciniak A., Wojcicka G., Gorny D.

Journal of Physiology and Pharmacology

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2003

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tom 54

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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.

8

Identification of a presynaptic cannabinoid CB1 receptor in the guinea-pig atrium and sequencing of the guinea-pig CB1 receptor

84%

Kurz C. M., Gottschalk C., Schlicker E., Kathmann M.

Journal of Physiology and Pharmacology

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2008

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tom 59

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nr 1

We studied whether cannabinoid CB1 receptors occur on the sympathetic neurones innervating the guinea-pig atrium and renal cortex. Atrial and cortical kidney pieces preincubated with [3H]-noradrenaline were superfused and the electrically (3 Hz)-evoked tritium overflow was examined. The evoked overflow in atrium was inhibited by the cannabinoid agonist WIN 55,212-2 maximally by 35%; its concentration-response curve was shifted to the right by the CB1 antagonist rimonabant (pA2 8.3), which, by itself, did not affect the evoked overflow. The evoked overflow in the renal cortex was not altered by WIN 55,212-2. The muscarinic agonist oxotremorine and prostaglandin E2 inhibited the evoked overflow maximally by 55 and 65% in atrium and by 80 and 55% in kidney, respectively. Furthermore, the nucleotide sequence of the guinea-pig CB1 receptor was determined (GenBank DQ355990). The deduced amino acid sequence has a high homology to the corresponding sequence of man (98.7%) and rat or mouse (99.2%). In conclusion, presynaptic CB1 receptors leading to inhibition of noradrenaline release occur in guinea-pig atrium but not renal cortex. The deduced amino acid sequence of the guinea-pig CB1 receptor shows a homology of 99% to the CB1 receptor sequence of rodents and humans.

9

Specific features and roles of renal circulation: angiotensin II revisited

67%

Sadowski J., Badzynska B.

Journal of Physiology and Pharmacology. Supplement

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2006

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tom 57

|

nr 11

169-178

The status of intrarenal circulation determines in part renal excretion, affects body fluid homeostasis and has a role in long term control of arterial blood pressure. The vascular resistance in the renal cortex and medulla is determined by interaction of a vast array of vasoactive hormones and paracrine factors; among these the role of constrictor angiotensin II and dilator prostaglandins and nitric oxide may appear to be dominating. The focus of this review and underlying studies is on the mechanisms whereby the microcirculation of the renal medulla is protected against the vasoconstrictor action of angiotensin II. In anaesthetized normal rats the three mentioned active agents or their inhibitors were applied and total renal blood flow and cortical, outer- and inner medullary laser-Doppler fluxes were determined; in some studies renal tissue nitric oxide was measured using selective electrodes. We conclude that angiotensin II, acting via AT1 receptors, constricts the renal cortical vasculature; in the medulla its action is effectively buffered by prostaglandin E2 but most probably not by nitric oxide.

10

Cell migration between graft and host - an analysis with monoclonal antibodies after allogeneic rat kidney transplantation

67%

Krzymanski M., Oko A., Waaga A. M., Zeromski J., Ulrichs K., Muller-Ruchholtz W.

Archivum Immunologiae et Therapiae Experimentalis

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1995

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tom 43

|

nr 3-4

Ograniczanie wyników

Variation of the structure and course of the interlobular arteries in human kidney

Variation of the structure and course of the interlobular arteries in human kidney

TGF-beta1 immunohistochemistry and promoter methylation in chronic renal failure rats treated with uremic clearance granules

Renal tissue NO and intrarenal haemodynamics during experimental variations of NO content in anaesthetised rats

The effects of indomethacin on angiogenic factors mRNA expression in renal cortex of healthy rats

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

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

Identification of a presynaptic cannabinoid CB1 receptor in the guinea-pig atrium and sequencing of the guinea-pig CB1 receptor

Specific features and roles of renal circulation: angiotensin II revisited

Cell migration between graft and host - an analysis with monoclonal antibodies after allogeneic rat kidney transplantation