title: Atrial natriuretic peptide inhibits osmotical glial cell swelling in the ischemic rat retina: dependence on glutamatergic-purinergic signaling.
abstract: Atrial natriuretic peptide (ANP) is a regulator of the water and electrolyte content in the brain which also mediates cell volume homeostasis. Here, we determined whether the expression of ANP in the retina of the rat undergoes changes during ischemia-reperfusion, and whether ANP affects the osmotic swelling of Müller glial cells in postischemic retinas under hypotonic conditions. Transient retinal ischemia was induced by elevation of the intraocular pressure above systolic blood pressure for 1h. At 1 and 3 days after reperfusion, there was an increased content of ANP protein in the retina, as determined by Western blotting. The increase of the retinal ANP content was markedly reduced when triamcinolone acetonide (10 mM in 2 microl vehicle) was intravitreally injected before ischemia. ANP inhibited the osmotic swelling of Müller cell somata in retinal slices. The effect of ANP was mediated by activation of NP receptors expressed by retinal neurons which evoked a release of glutamate. The stimulation of metabotropic glutamate receptors expressed by Müller cells evoked an autocrine purinergic signaling mechanism that resulted in the opening of K(+) and Cl(-) channels; the ion efflux counteracted the osmotic swelling of Müller cells. It is concluded that the expression of ANP is transiently upregulated in the postischemic retina of the rat. The increased expression of ANP may represent a part of the retinal response to transient ischemia and may inhibit cytotoxic glial cell swelling.
authors.affiliation: Paul Flechsig Institute of Brain Research, University of Leipzig Medical Faculty, 04109 Leipzig, Germany.
authors.forename: Folke
authors.initials: F
authors.lastname: Kalisch
authors.forename: Antje
authors.initials: A
authors.lastname: Wurm
authors.forename: Ianors
authors.initials: I
authors.lastname: Iandiev
authors.forename: Ortrud
authors.initials: O
authors.lastname: Uckermann
authors.forename: Nihat
authors.initials: N
authors.lastname: Dilsiz
authors.forename: Andreas
authors.initials: A
authors.lastname: Reichenbach
authors.forename: Peter
authors.initials: P
authors.lastname: Wiedemann
authors.forename: Andreas
authors.initials: A
authors.lastname: Bringmann
mesh_terms: D000818:Animals; D009320:Atrial Natriuretic Factor / Q000378:metabolism / Q000502:physiology*; D019898:Autocrine Communication / Q000502:physiology; D002118:Calcium / Q000502:physiology; D048429:Cell Size; D009457:Neuroglia / Q000473:pathology* / Q000502:physiology; D051381:Rats; D020318:Rats, Long-Evans; D017470:Receptors, Glutamate / Q000378:metabolism; D011983:Receptors, Purinergic / Q000235:genetics / Q000378:metabolism; D015427:Reperfusion Injury / Q000378:metabolism / Q000473:pathology* / Q000503:physiopathology; D012171:Retinal Vessels / Q000378:metabolism / Q000473:pathology*; D015533:Transcriptional Activation
chemical_list: D017470:Receptors, Glutamate; D011983:Receptors, Purinergic; D009320:Atrial Natriuretic Factor; D002118:Calcium