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  • Title: Characterization of atrial natriuretic factor receptors in human glomerular epithelial and mesangial cells.
    Author: Chansel D, Pham P, Nivez MP, Ardaillou R.
    Journal: Am J Physiol; 1990 Oct; 259(4 Pt 2):F619-27. PubMed ID: 2171358.
    Abstract:
    To evaluate the distribution and functions of receptors of atrial natriuretic factor (ANF) in human glomeruli, we studied the binding sites of ANF-(1-28) in homogeneous populations of human glomerular epithelial cells or mesangial cells. 125I-labeled ANF bound specifically to both cell types. Equilibrium saturation binding curves suggested one group of receptor sites in mesangial cells (Kd = 99 +/- 32 pmol/l, Bmax = 15.3 +/- 3.5 fmol/mg) but multiple groups in glomerular epithelial cells. Binding was greater at 37 than at 4 degrees C in mesangial cells. The reverse was observed in glomerular epithelial cells due to marked degradation of the tracer at 37 degrees C. The fractions of undisplaceable tracer in a hypertonic acid medium after 60 min incubation were 45 and 16% at 37 degrees C for glomerular epithelial and mesangial cells, respectively. ANF-(1-28) and C-ANF-(4-23), a specific ligand of clearance receptors, similarly inhibited 125I-ANF binding to mesangial cells, whereas [Ala7-Ala23]-ANF, a linear analogue, was slightly less potent. In epithelial cells, C-ANF-(4-23) competitively inhibited 125I-ANF binding but with a lower potency than ANF, whereas linear ANF at low concentrations (10-100 pmol/l) stimulated 125I-ANF binding. In addition, linear ANF markedly inhibited the degradation of 125I-ANF in the incubation medium of epithelial and mesangial cells, whereas thiorphan, an inhibitor of enkephalinase, was inactive. ANF-(1-28) stimulated cGMP production in glomerular epithelial cells but not in mesangial cells. Both analogues were inactive in both cell types and did not modify ANF-(1-28)-dependent cGMP synthesis.(ABSTRACT TRUNCATED AT 250 WORDS)
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