Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0403608 (ureter)
 9,655 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Circulating factors, including the plasma protease (100 KF) described previously, have been suspected to play a role in the pathogenesis of minimal change disease (MCD) for several decades. This factor was able to induce MCD-like alterations in kidney tissue in vitro, i.e. impairment of glomerular polyanion (GPA), as well as glomerular ecto-ATPase. We conducted permeability studies using alternate perfusion of the rat kidney ex vivo according to standard techniques. Either native 100 KF (n = 7) or control factor (n = 7) perfusion, followed by perfusion with diluted rat serum was carried out, while urine samples were collected by ureter cannulation. Total urinary protein (by spectrophotometry) as well as IgG (by ELISA) and albumin (by rocket electrophoresis) were measured. Sections of perfused kidneys were stained (immuno-) histochemically for GPA and glomerular ecto-ATPase, and the stainability was quantified using image analysis and expressed as arbitrary units. The results show significantly increased protein leakage after perfusion of 100 KF versus control factor (150.0 +/- 48.9 vs. 33.2 +/- 7.7 micrograms/min, p < or = 0.01), while the IgG/albumin ratio has decreased (12.0 +/- 9.4 vs 26.9 +/- 14.4%, p < or = 0.01). Plasma protein leakage after 100KF perfusion is associated with a significant loss of GPA (57.3 +/- 27.5 vs. 98.4 +/-12.0, p < or = 0.01) and significant decrease of glomerular ecto-ATPase expression (28.7 +/- 11.5 vs. 79.5 +/- 15.0, p < or = 0.001). The capability of 100KF to induce MCD-like glomerular lesions, in association with selectively increased permeability for plasma proteins, suggests that this human plasma constituent may be important in the pathogenesis of MCD.
 ...
PMID:Minimal change-like glomerular alterations induced by a human plasma factor. 893 86

This study was conducted to determine whether adenosine 5'-triphosphate (ATP) contributes to nociceptor activity induced by ureter distension. Multifibre recordings of ureter afferents were made using the guinea pig ureter preparation perfused in vitro. Distension of the ureter resulted in an initial rapid and later maintained increase in afferent nerve discharge. Intraluminal application of ATP (10-1000 microM, 0.1 ml/min for 3 min) or alpha,beta-meATP (10-1000 microM) mimicked these increases in afferent activity. The afferent responses consisted of fast and slow components. Both agonists caused a sensitisation of the afferents to ureter distensions. TNP-ATP (30 microm), a P2X3 receptor antagonist, and the non-specific P2 antagonist, PPADS (100 microm), blocked the rapid and reduced the slower response to ATP. The remaining responses were blocked by the selective A1 receptor antagonist, DPCPX. TNP-ATP and PPADS reduced distension-induced afferent activity. The selective ecto-ATPase inhibitor, ARL-67156 (100, 200 microM) and suramin (100, 200 microM), an ecto-nucleotidase inhibitor as well as a P2 receptor antagonist, produced an increase in baseline and distension-induced discharge. These results indicate that the ureter epithelium may tonically (at rest) as well as phasically (on distension) release ATP, which stimulates afferent terminals by interacting with multiple P2 and P1 receptors.
 ...
PMID:Activation of ureter nociceptors by exogenous and endogenous ATP in guinea pig. 1555 43