scholarly journals Collagen studies in newborn rat kidneys with incomplete ureteric obstruction

1993 ◽  
Vol 44 (3) ◽  
pp. 593-605 ◽  
Author(s):  
Anna Haralambous-Gasser ◽  
Danny Chan ◽  
Rowan G. Walker ◽  
Harley R. Powell ◽  
Gavin J. Becker ◽  
...  
2004 ◽  
Vol 25 (3) ◽  
pp. 216-227 ◽  
Author(s):  
Athina Pyrpasopoulou ◽  
Vassiliki Kotoula ◽  
Angeliki Cheva ◽  
Prodromos Hytiroglou ◽  
Eleni Nikolakaki ◽  
...  

1986 ◽  
Vol 103 (6) ◽  
pp. 2489-2498 ◽  
Author(s):  
D R Abrahamson ◽  
E W Perry

Tannic acid in glutaraldehyde fixatives greatly enhanced the visualization of two developmentally and morphologically distinct stages in glomerular basement membrane (GBM) formation in newborn rat kidneys. First, in early stage glomeruli, double basement membranes between endothelial cells and podocytes were present and, in certain areas, appeared to be fusing. Second, in maturing stage glomeruli, elaborate loops and outpockets of basement membrane projected into epithelial, but not endothelial, sides of capillary walls. When Lowicryl thin sections from newborn rat kidneys were sequentially labeled with rabbit anti-laminin IgG and anti-rabbit IgG-colloidal gold, gold bound across the full width of all GBMs, including double basement membranes and outpockets. The same distribution was obtained when sections from rats that received intravenous injections of rabbit anti-laminin IgG 1 h before fixation were labeled directly with anti-rabbit IgG-colloidal gold. When kidneys were fixed 4 d after anti-laminin IgG injection, however, loops beneath the podocytes in maturing glomeruli were usually unlabeled and lengths of unlabeled GBM were interspersed with labeled lengths. In additional experiments, rabbit anti-laminin IgG was intravenously injected into newborn rats and, 4-14 d later, rats were re-injected with sheep anti-laminin IgG. Sections were then doubly labeled with anti-rabbit and anti-sheep IgG coupled to 10 and 5 nm colloidal gold, respectively. Sheep IgG occurred alone in outpockets of maturing glomeruli and also in lengths of GBM flanked by lengths containing rabbit IgG. These results indicate that, after fusion of double basement membranes, new segments of GBM appear beneath developing podocytes and are subsequently spliced into existing GBM. This splicing provides the additional GBM necessary for expanding glomerular capillaries.


1976 ◽  
Vol 15 (06) ◽  
pp. 282-286 ◽  
Author(s):  
M. Rembelska ◽  
M. Ogiński

SummaryThe investigations were carried out with a newly syn-thesised, original 99mTc-Unithiol complex (Unithiol-2,3-dimercaptopropansulphonate). It accumulates in the kidneys and enables their scintigraphic examination at 90—180 minutes after the administration. The study was performed on rats, rabbits and dogs. 99mTc-Unithiol complex accumulation in rat kidneys was 34,9%, 44,5% and 67,8% of dose after 1, 2 and 3 h respectively.Good reability of the scintigraphic picture of the kidneys in rabbits and dogs confirms the accumulative capability of the complex in these organs. It was found by means of ascending paper chromatography that the purity of the 99mTc-Unithiol complex exceeded 90%.


1980 ◽  
Vol 93 (3) ◽  
pp. 339-345 ◽  
Author(s):  
Naokazu Nagata ◽  
Yuriko Ono ◽  
Narimichi Kimura

Abstract. The interaction between parathyroid hormone (PTH) and prostaglandin E1 (PGE1) in influencing cyclic AMP metabolism in rat renal cortical tissue was examined. PTH and PGE1 stimulated additively the adenylate cyclase activity in the homogenate of the tissue. Both PTH and PGE1 enhanced the level of cyclic AMP in the incubated renal cortical tissue, but the effect of their simultaneous addition did not exceed the effect induced by PTH alone. Cyclic AMP accumulated in the incubation medium by stimulation by PTH was decreased by the simultaneous addition of PGE1. When the tissue was pre-incubated for 30 min with 2 to 10 μg/ml of PGE1, the magnitude of the increase of cyclic AMP caused by PTH subsequently added was lessened. However, the response to PTH of adenylate cyclase preparation obtained from the homogenate of PGE1-pre-treated tissue was not decreased. When first PTH was added to the incubating renal cortical tissue, the subsequent addition of PGE1 accelerated the decrease of cyclic AMP content in the tissue and decreased the amount of cyclic AMP released from the tissue. The interaction of PTH and PGE1 on cyclic AMP metabolism in the renal cortical tissue was in contrast to that seen in newborn rat calvaria where PGE1 and PTH acted additively in enhancing the level of cyclic AMP.


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