Regulation of renin gene expression in kidneys of eNOS- and nNOS-deficient mice
dc.contributor.author | Schrader, J. | en_US |
dc.contributor.author | Gödecke, A. | en_US |
dc.contributor.author | Ford, M. | en_US |
dc.contributor.author | Kurtz, A. | en_US |
dc.contributor.author | Schnermann, Jürgen B. | en_US |
dc.contributor.author | Wagner, C. | en_US |
dc.date.accessioned | 2006-09-08T20:07:32Z | |
dc.date.available | 2006-09-08T20:07:32Z | |
dc.date.issued | 2000-03 | en_US |
dc.identifier.citation | Wagner, C.; Gödecke, A.; Ford, M.; Schnermann, J.; Schrader, J.; Kurtz, A.; (2000). "Regulation of renin gene expression in kidneys of eNOS- and nNOS-deficient mice." Pflügers Archiv 439(5): 567-572. <http://hdl.handle.net/2027.42/42244> | en_US |
dc.identifier.issn | 0031-6768 | en_US |
dc.identifier.uri | https://hdl.handle.net/2027.42/42244 | |
dc.identifier.uri | http://www.ncbi.nlm.nih.gov/sites/entrez?cmd=retrieve&db=pubmed&list_uids=10764216&dopt=citation | en_US |
dc.description.abstract | Our study aimed to assess the roles of nitric oxide derived from endothelium NO-synthase (eNOS) and macula densa neuronal NO-synthase (nNOS) in the regulation of renal renin expression. For this purpose renin mRNA levels and renin content were determined in kidneys of wild-type (wt), nNOS-deficient (nNOS–/–), and eNOS-deficient (eNOS–/–) mice, in which the renin system was suppressed by feeding a high-salt diet (NaCl 4%), or was stimulated by feeding a low-salt (NaCl 0.02%) diet together with the converting-enzyme inhibitor ramipril (10 mg kg –1 day –1 ). In all mouse strains, renin mRNA levels were inversely related to the rate of sodium intake. In eNOS–/– mice renin mRNA levels and renal renin content were 50% lower than in wt mice at each level of salt intake, whilst in nNOS–/– mice renin expression was not different from wt controls. Administration of the general NO-synthase inhibitor nitro- l -arginine methyl ester ( l -NAME, 50 mg kg –1 day –1 ) to mice kept on the low-salt/ramipril regimen caused a decrease of renal renin mRNA levels in wt and nNOS–/– mice, but not in eNOS–/– mice. These observations suggest that neither eNOS nor nNOS is essential for up- or downregulation of renin expression. eNOS-derived NO appears to enhance renin expression, whereas nNOS-derived NO does not. | en_US |
dc.format.extent | 140040 bytes | |
dc.format.extent | 3115 bytes | |
dc.format.mimetype | application/pdf | |
dc.format.mimetype | text/plain | |
dc.language.iso | en_US | |
dc.publisher | Springer-Verlag | en_US |
dc.subject.other | MRNA NO Synthase Inhibition NO Synthase Knockout Renin Renin Content | en_US |
dc.subject.other | Legacy | en_US |
dc.title | Regulation of renin gene expression in kidneys of eNOS- and nNOS-deficient mice | en_US |
dc.type | Article | en_US |
dc.subject.hlbsecondlevel | Physiology | en_US |
dc.subject.hlbtoplevel | Health Sciences | en_US |
dc.description.peerreviewed | Peer Reviewed | en_US |
dc.contributor.affiliationum | Department of Physiology, University of Michigan, Ann Arbor, MI 48109, USA, | en_US |
dc.contributor.affiliationum | Department of Physiology, University of Michigan, Ann Arbor, MI 48109, USA, | en_US |
dc.contributor.affiliationother | Institut für Physiologie I, Universität Regensburg, D-93040 Regensburg, Germany, | en_US |
dc.contributor.affiliationother | Institut für Herz- und Kreislaufphysiologie, Heinrich-Heine-Universität, Düsseldorf, D-40001 Düsseldorf, Germany, | en_US |
dc.contributor.affiliationother | Institut für Physiologie I, Universität Regensburg, D-93040 Regensburg, Germany, | en_US |
dc.contributor.affiliationother | Institut für Herz- und Kreislaufphysiologie, Heinrich-Heine-Universität, Düsseldorf, D-40001 Düsseldorf, Germany, | en_US |
dc.contributor.affiliationumcampus | Ann Arbor | en_US |
dc.identifier.pmid | 10764216 | en_US |
dc.description.bitstreamurl | http://deepblue.lib.umich.edu/bitstream/2027.42/42244/1/424-439-5-567_s004249900214.pdf | en_US |
dc.identifier.doi | http://dx.doi.org/10.1007/s004249900214 | en_US |
dc.identifier.source | Pflügers Archiv | en_US |
dc.owningcollname | Interdisciplinary and Peer-Reviewed |
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