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1

Histopathological examination of renal glomerules in cattle infected with bovine leukemia virus

100%
Rotkiewicz T., Otrocka-Domagala I., Babinska I.
Polish Journal of Natural Sciences
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2003
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tom 14
2
Content available remote

Inhibitory effect of Ca2+ on ATP-mediated stimulation of NPR-A-coupled guanylyl cyclase in renal glomeruli from spontaneously hypertensive and normotensive rats

86%
Woodard G. E., Zhao J., Rosado J. A.
Journal of Physiology and Pharmacology
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2006
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tom 57
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nr 3
Atrial natriuretic peptide (ANP) regulates blood pressure mainly through the occupation of the guanylyl cyclase-coupled receptor NPR-A, which requires ATP interaction for maximal activation. This study investigates the effect of extracellular Ca2+ on ATP-mediated regulation of NPR-A-coupled guanylyl cyclase activity in glomerular membranes from Wistar Kyoto (WKY) and spontaneously hypertensive rats (SHR). ATP induced a significant increase in basal and ANP1-28-stimulated guanylyl cyclase activity that was greater in SHR than in WKY. Extracellular Ca2+ inhibited ATP-stimulated guanylyl cyclase activity in a concentration-dependent manner, but did not modify basal and ANP1-28-stimulated guanylyl cyclase activity. In the presence of ATP, NPR-A showed higher affinity for ANP1-28 and lower Bmax. Ca2+ did not modify NPR-A-ANP1-28 binding properties. The different effects of extracellular Ca2+ on ANP1-28- or ATP-mediated guanylyl cyclase activation suggest that these events are differentially regulated. Addition of extracellular Ca2+ induced similar effects in hypertensive and normotensive rats, suggesting that it is not responsible for the elevated cGMP production observed in SHR.
3
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Co-operation between particulate and soluble guanylyl cyclase systems in the rat renal glomeruli

72%
Stepinski J., Wendt U., Lewko B., Angielski S.
Journal of Physiology and Pharmacology
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2000
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tom 51
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nr 3
4
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Bidirectional action of extracellular ATP on intracapillary volume of isolated rat renal glomeruli

72%
Jankowski M., Szczepanska-Konkel M., Kalinowski L., Angielski S.
Journal of Physiology and Pharmacology
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2000
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tom 51
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nr 3
5
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Responsiveness of renal glomeruli to adenosine in streptozotocin-induced diabetic rats dependent on hyperglycaemia level

72%
Szczepanska-Konkel M., Jankowski M., Stiepanov-Trzeciak A., Rudzik A., Pawelczyk T., Angielski S.
Journal of Physiology and Pharmacology
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2003
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tom 54
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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.
6
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Effect of cAMP analogues on glomerular inulin space of isolated rats renal glomeruli

72%
Van Bemmelen M. X. P., Szczepanska-Konkel M., Jastorff B., Jankowski M., Angielski S.
Journal of Physiology and Pharmacology
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2005
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tom 56
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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.
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