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1

Role of P1 and P2 purinoceptors in the regulation of glomerular filtration rate

100%
Szczepanska-Konkel M.
Acta Biochimica Polonica
|
2003
|
tom 50
|
nr Supplement 1
2

Heterogenity of precipitation subfractions of HDL

51%
Kortas-Stempak B., Wroblewska M., Badzio T., Szczepanska-Konkel M.
Acta Biochimica Polonica
|
2003
|
tom 50
|
nr Supplement 1
3

Chronic kidney denervation induces hypersensitivity to agonist of P2X receptors and increases expression of P2X1 receptor mRNA

51%
Jankowski M.-W., Kowalski R., Szczepanska-Konkel M.
Acta Biochimica Polonica
|
2007
|
tom 54
|
nr Supplement 4
4

Adeonosine concentration in diabetic rat renal interstitium

51%
Kowalski R., Stiepanow-Trzeciak A., Jankowski M., Szczepanska-Konkel M.
Acta Biochimica Polonica
|
2006
|
tom 53
|
nr Supplement 1
5
Artykuł dostępny w postaci pełnego tekstu - kliknij by otworzyć plik
Content available

Znaczenie gospodarki kwasowo-zasadowej w oporności na fosfaturyczne działanie parathormonu u szczurów traktowanych litem

51%
Szczepanska-Konkel M., Drewnowska K., Pempkowiak L., Angielski S.
Diagnostyka Laboratoryjna
|
1980
|
tom 16
|
nr 2
6

The effect of calcium restriction in the diet on calcium transport in rat small intestine

51%
Michalska L., Wrobel J., Szczepanska-Konkel M.
Acta Biochimica Polonica
|
1976
|
tom 23
|
nr 2-3
7

Effect of dipyridamole and furosemide on rental function during adenine dinucleotide infusion in rats

51%
Redlak M., Szczepanska-Konkel M., Stepinski J., Angielski S.
Acta Physiologica Polonica
|
1986
|
tom 37
|
nr 1
8

Ap4A modifies renal function by P2 purinoreceptors

51%
Stiepanow-Trzeciak A., Rudzik A., Szczepanska-Konkel M.
Acta Biochimica Polonica
|
2003
|
tom 50
|
nr Supplement 1
9
Artykuł dostępny w postaci pełnego tekstu - kliknij by otworzyć plik
Content available

Bidirectional action of extracellular ATP on intracapillary volume of isolated rat renal glomeruli

51%
Jankowski M., Szczepanska-Konkel M., Kalinowski L., Angielski S.
Journal of Physiology and Pharmacology
|
2000
|
tom 51
|
nr 3
10
Content available remote

Dissociation between the effects of P1,P4-diadenosine tetraphosphate (Ap4A) on renal haemodynamics and tubular function in anaesthetized rats

51%
Jankowski M., Angielski S., Szczepanska-Konkel M.
Journal of Physiology and Pharmacology
|
2008
|
tom 59
|
nr 1
Previous studies from our laboratory have reported a marked reduction in glomerular filtration rate (GFR) and sodium reabsorption in renal proximal tubule during intravenous infusion of P1,P4-diadenosine tetraphosphate (Ap4A) at dose of 1.0 µmol/kg + 10 nmol/kg/min (i.v., injection followed by infusion) in anaesthetized Wistar rats. In the present study, the changes of GFR and urine sodium excretion were investigated in response to systemic infusion of Ap4A at different doses. Ap4A at dose of 0.1 µmol/kg + 1.0 nmol/kg/min did not change GFR and sodium urinary excretion whereas 2-fold higher dose produced significant (3.4-fold) increase in sodium excretion without changes in GFR. Significant but transient reduction in GFR by ~21% was observed during infusion of Ap4A at dose of 0.5 µmol/kg + 5.0 nmol/kg/min. Higher doses of Ap4A (1.0 µmol/kg + 10 nmol/kg/min and 2.0 µmol/kg + 20 nmol/kg/min) produced sustained reduction in GFR and marked natriuresis. Our results suggest that tubular sodium transport systems are more sensitive to Ap4A than systems involved in GFR regulation.
11
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Ostra niewydolność nerek wywołana dinukleotydem nikotynamido-adeninowym

45%
Angielski S., Madrala A., Pawlowska D., Redlak M., Szczepanska-Konkel M.
Diagnostyka Laboratoryjna
|
1984
|
tom 20
|
nr 1
12
Content available remote

Effect of cAMP analogues on glomerular inulin space of isolated rats renal glomeruli

45%
Van Bemmelen M. X. P., Szczepanska-Konkel M., Jastorff B., Jankowski M., Angielski S.
Journal of Physiology and Pharmacology
|
2005
|
tom 56
|
nr 1
Cyclic AMP has been generally recognised as activator of cAMP-dependent protein kinases. However, there is little evidence about role of cAMP-dependent protein kinase (PKA), in particular izoenzymes PKA-I and PKA-II, in glomeruli contractility. We measured changes of glomerular inulin space (GIS) as a marker of its contractility in the presence of phosphodiesterase resistance cAMP analogues; activators and inhibitors of PKA. Activator of PKA i.e. (Sp) 8-Cl-cAMPS (0.1-100 µM) decreased GIS. (Rp) 8-Cl-cAMPS (0.1-100 µM), inhibitor of PKA, was ineffective but shifted concentration-response curve of (Sp) 8-Cl-cAMPS to right at 50 µM. Specific A site activation by N6-benzoyl-cAMP decreased GIS with maximum at 0.1 µM. Activation of B site by 8-aminobutyloamino-cAMP (0.1-100 µM) had no effect. However, specific activation of both sites on PKA-I or PKA-II by site-selective analogue pairs e.g. 8-aminobutyloamino-cAMP plus 8-piperidino-cAMP or N6-benzoyl-cAMP plus 8-piperidino-cAMP respectively, significantly increased sensitivity of glomeruli to analogues. Our data suggest that activation of PKA-I or PKA-II might have an important role in the regulation of glomerular contractility.
13
Content available remote

Renal haemodynamics and natriuretic responses to intravenous administration of diadenosine tetraphosphate [AP4A] and nicotinamide adenine dinucleotide [NAD] in rat

39%
Szczepanska-Konkel M., Langner G., Bednarczuk G., Stiepanow-Trzeciak A., Jankowski M., Angielski S.
Journal of Physiology and Pharmacology
|
2003
|
tom 54
|
nr 2
Effects of Ap4A and NAD - precursor of adenosine, on renal plasma flow (RPF), glomerular filtration rate (GFR) and urine excretion were determined in the anaesthetised rats. Infusion of Ap4A or NAD (i.v., bolus - 1 µmol/kg followed by 10 nmol/min/kg) decreased RPF and GFR (by 30 and 40%, respectively). In spite of GFR reduction during Ap4A infusion, the significant increase in sodium excretion and urine flow was noticed: fractional sodium (FENa) and urine excretion (FEurine) rose 15-fold and 2.5-fold in comparision with the control value, respectively. In contrast to Ap4A, NAD-induced decrease in GFR was associated with parallel decrease in sodium and urine excretion, thus the FENa and FEurine did not significantly change. Pre-treatment with adenosine deaminase (adenosine degrading enzyme, 2 U/min/kg) or theophylline (P1-receptors antagonist, 0.2 mmol/min/kg) ceased responses to NAD, wherease Ap4A-induced changes were not affected. Pre-treatment with suramin (P2-receptors antagonist, (i.v., bolus - 12 mg/kg followed by 1.2 mg/min/kg) completely abolished the renal effects of Ap4A. We conclude that Ap4A may exert specific action on renal function. It acts different from NAD that modified renal function through its hydrolysis product - adenosine. Ap4A might reduce glomerular filtration rate and evoke natriuresis and diuresis, and its effects are probably mediated through stimulation of P2-receptors.
14
Content available remote

Responsiveness of renal glomeruli to adenosine in streptozotocin-induced diabetic rats dependent on hyperglycaemia level

39%
Szczepanska-Konkel M., Jankowski M., Stiepanov-Trzeciak A., Rudzik A., Pawelczyk T., Angielski S.
Journal of Physiology and Pharmacology
|
2003
|
tom 54
|
nr 1
Glomerular filtration rate (GFR) in response to adenosine precursor, NAD, and glomeruli contractility in response to adenosine were evaluated in streptozotocin-induced diabetic rats with severe (blood glucose 27.8±1.2 mmol/L) and moderate hyperglycaemia (18.2±0.9 mmol/L) compared with nondiabetic (ND)-rats. In anaesthetised rats, basal GFR was greater in moderately diabetic rats compared with severely diabetic rats (p<0.05) and ND-rats (p<0.02). Intravenous infusion of 5 nmol·min-1·kg-1 NAD reduced GFR and renal plasma flow (RPF) in diabetic rats but had no effect on these parameters in ND-rats. Moreover, NAD-induced reduction of GFR and RPF was greater in rats with severe diabetes (41% and 30%, respectively) than in with moderate diabetes (25% and 26%, respectively). Theophylline (0.2 µmol·min-1·kg-1) abolished renal response to NAD. Isolated glomeruli contraction in response to adenosine, assessed by glomerular 3H-inulin space reduction, was lowered in moderately diabetic-group and enhanced in severely diabetic-group, compared with ND-group (p<0.05). Adenosine A1-receptor antagonist DPCPX inhibited adenosine-induced glomeruli contraction. This differential response of diabetic renal glomeruli to adenosine suggests that impaired glomerular contractility in response to adenosine could be responsible for hyperfiltration in moderate diabets, whereas, the increased adenosine-dependent contractility of glomeruli in severe diabetes may increase the risk of acute renal failure in this condition.
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