Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P41181 (collecting duct)
 5,183 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Morphological changes were followed in semi-thin glycolmethacrylate sections, after treating male Wistar rats with a single ip dose of 2-bromoethanamine (BEA) hydrobromide (100 mg/kg) to induce renal papillary necrosis. Medullary interstitial cells had irregular nuclei at 4 hr and focal necrosis by 8 hr which spread from the papilla tip to the cortico-medullary junction from 12 hr. Increased mucopolysaccharide staining was observed in the papilla tip at 4 hr, and was lost from those regions where necrosis had developed by 48 hr. Endothelial platelet adhesion, first seen at 8 hr, was very marked at 18 hr, but affected capillaries in necrotic regions only, up to 144 hr. The absence of extravasated Monastral Blue B demonstrated the integrity of the medullary microvascular endothelia. The distal nephron showed degenerative changes at 12 hr and cell exfoliation at 18 hr. Cortical changes were confined to PAS-positive casts in the collecting duct and loop of Henle from 8 hr and dilatation of distal and proximal tubules at 8 and 72 hr, respectively. There was active repair at the junction between viable and necrotic tissue in the papilla from 24 hr with mitoses in the collecting ducts and loops of Henle. Normally the urothelium is less than 3-4 cells thick, but upper urothelial proliferation followed BEA administration. Hyperplasia was especially marked at the mouth of the ureter and in the pelvis opposite the region of necrosis (7-8 cells thick at 18 hr) and had only partially resolved by 144 hr.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:High resolution light microscopic morphological and microvascular changes in an acutely induced renal papillary necrosis. 219 75

The mature, fully differentiated cortical collecting duct plays a major role in the final renal regulation of Na+, K+ and H+ transport. To characterize the growth of this segment, we measured the outer diameter and the dry weight of cortical collecting ducts isolated from newborn, 1-month-old, and adult rabbits. During the 1st month of life no significant changes were observed; however, there was a 60% increase in both parameters after the 4th week of life. Growth-related accretion of K+ was demonstrated by showing tubular K+ content to increase by 60% with maturation. Concomitant with the increase in tubular size, total cell number per millimeter of tubular length rose by 30%. Approximately 50% of the observed increment in tubular size could be accounted for by cell hyperplasia, with the remaining increase resulting from cell hypertrophy. Hypertrophy of principal cells was confirmed by scanning electron microscopy, which demonstrated a doubling of the circumferential width without any change in longitudinal length. Hyperplasia was confirmed, using a fluorescent chromatin stain, by our finding of a mitotic frequency of 3/1000 cells in the neonatal mid-cortical collecting duct; the observed number of mitoses was 10-fold higher at the most cortical end (ampulla). The number of intercalated cells per millimeter of tubule length, identified by bright green fluorescence after cortical collecting ducts were stained with 6-carboxyfluorescein diacetate, was found to double during maturation, the increase being significant only after the 4th postnatal week. We conclude that maturation of the mid-cortical collecting duct results from both cellular hyperplasia and hypertrophy. It is unlikely that this segment plays a major role in regulating Na+, K+, and H+ transport in the neonatal kidney.
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PMID:Postnatal maturation of the rabbit cortical collecting duct. 315 87