Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
10
pubmed:dateCreated
1999-11-9
pubmed:abstractText
Prostaglandins participate in the regulation of important glomerular functions and are involved in the pathogenesis of glomerular diseases. This study investigates the influence of prostaglandins on membrane voltage, ion conductances, cAMP accumulation, and cytosolic calcium activity ([Ca2+]i) in differentiated podocytes. Prostaglandin E2 (PGE2) caused a concentration-dependent depolarization and an increase of the whole cell conductance in podocytes (EC50 approximately 50 nM). Compared with PGE2, the EP2/EP3/EP4 receptor agonist 11-deoxy-PGE1 caused an equipotent depolarization, whereas the DP receptor agonist BW 245 C, the EP1/EP3 receptor agonist sulprostone, and the IP receptor agonist iloprost were at least 100 to 1000 times less potent than PGE2. The EP2 receptor agonist butaprost did not change membrane voltage of podocytes. The depolarizing effect of PGE2 was increased in an extracellular solution with a reduced Cl- concentration (from 145 to 32 mM). PGE2 and the prostaglandin agonists, but not the IP receptor agonist iloprost and the EP2 receptor agonist butaprost, induced a time- and concentration-dependent cAMP accumulation in podocytes. In fura-2 fluorescence experiments, PGE2, sulprostone, PGF2alpha, fluprostenol (a potent FP agonist), and U-46619 (a selective thromboxane A2 agonist) induced a biphasic increase of [Ca2+]i in 60 to 80% of podocytes. In reverse transcription-PCR studies, podocyte mRNA for the EP1, EP4, FP, and TP receptor could be amplified. These data indicate that in podocytes, PGE2 regulates distinct cellular functions via the EP1 and EP4 receptor, thereby increasing [Ca2+]i and cAMP, respectively. Furthermore, PGF1alpha and U-46619 increase [Ca2+]i via their specific receptors.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Oct
pubmed:issn
1046-6673
pubmed:author
pubmed:issnType
Print
pubmed:volume
10
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
2084-93
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:10505684-15-Hydroxy-11 alpha,9..., pubmed-meshheading:10505684-Animals, pubmed-meshheading:10505684-Base Sequence, pubmed-meshheading:10505684-Calcium Isotopes, pubmed-meshheading:10505684-Cell Membrane, pubmed-meshheading:10505684-Cells, Cultured, pubmed-meshheading:10505684-Cyclic AMP, pubmed-meshheading:10505684-Dinoprost, pubmed-meshheading:10505684-Dinoprostone, pubmed-meshheading:10505684-Endothelium, pubmed-meshheading:10505684-Ion Transport, pubmed-meshheading:10505684-Kidney Glomerulus, pubmed-meshheading:10505684-Mice, pubmed-meshheading:10505684-Molecular Sequence Data, pubmed-meshheading:10505684-Patch-Clamp Techniques, pubmed-meshheading:10505684-Polymerase Chain Reaction, pubmed-meshheading:10505684-RNA, Messenger, pubmed-meshheading:10505684-Radioimmunoassay, pubmed-meshheading:10505684-Receptors, Prostaglandin E, pubmed-meshheading:10505684-Sensitivity and Specificity
pubmed:year
1999
pubmed:articleTitle
Characterization of prostanoid receptors in podocytes.
pubmed:affiliation
Department of Medicine, University of Freiburg, Germany.
pubmed:publicationType
Journal Article, Comparative Study, Research Support, Non-U.S. Gov't