Machura, Katharina and Steppan, Dominik and Neubauer, Bjoern and Alenina, Natalia and Coffman, Thomas M. and Facemire, Carie S. and Hilgers, Karl F. and Eckardt, Kai-Uwe and Wagner, Charlotte and Kurtz, Armin (2009) Developmental renin expression in mice with a defective renin-angiotensin system. AMERICAN JOURNAL OF PHYSIOLOGY-RENAL PHYSIOLOGY, 297 (5). F1371-F1380. ISSN 1931-857X, 1522-1466
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Machura K, Steppan D, Neubauer B, Alenina N, Coffman TM, Facemire CS, Hilgers KF, Eckardt K, Wagner C, Kurtz A. Developmental renin expression in mice with a defective renin-angiotensin system. Am J Physiol Renal Physiol 297: F1371-F1380, 2009. First published August 26, 2009; doi: 10.1152/ajprenal.00378.2009.-During nephrogenesis, renin expression shifts from the vessel walls of interlobular arteries to the terminal portions of afferent arterioles in a wavelike pattern. Since the mechanisms responsible for the developmental deactivation of renin expression are as yet unknown, we hypothesized that the developing renin-angiotensin system (RAS) may downregulate itself via negative feedback to prevent overactivity of renin. To test for a possible role of angiotensin II in the developmental deactivation of renin expression, we studied the development of intrarenal renin expression in mice lacking ANG II AT(1a), AT(1b), or AT(2) receptors and in animals with abolished circulating ANG II due to deletion of the gene for angiotensin I-converting enzyme (ACE). The development of intrarenal renin expression was normal in mice lacking ANG II AT(1b) or AT(2) receptors. In animals lacking both ANG II AT(1a) and AT(1b) receptors, ACE, or ANG II AT(1a) receptors, renin expression was normal early and renin disappeared from mature vessels until development of cortical interlobular and afferent arterioles began. The development of cortical vessels in these genotypes was accompanied by a markedly increased number of renin-expressing cells, many of which were ectopically located and attached in a grapelike fashion to the outer vessel perimeter. Although the number of renin-expressing cells declined during final maturation of the kidneys, the atypical distribution pattern of renin cells was maintained. These findings suggest that ANG II does not play a central role in the typical developmental shift in renin expression from the arcuate vessels to the afferent arterioles. During postnatal maturation of mouse kidneys, interruption of the RAS causes severe hyperplasia of renin cells via a mechanism that centrally involves AT(1a) receptors. However, the distribution pattern of renin cells in adult kidneys with an interrupted RAS does not mimic any normal developmental stage since renin expression is frequently found in cells outside the arteriolar vessel walls in RAS mutants.
| Item Type: | Article |
|---|---|
| Uncontrolled Keywords: | RECEPTOR NULL MICE; BLOOD-PRESSURE; DEFICIENT MICE; JUXTAGLOMERULAR CELLS; CONVERTING ENZYME; GENE-EXPRESSION; MUTANT MICE; KIDNEY; LACKING; 1A; development; angiotensin II |
| Subjects: | 500 Science > 570 Life sciences |
| Divisions: | Biology, Preclinical Medicine > Institut für Physiologie > Prof. Dr. Armin Kurtz |
| Depositing User: | Dr. Gernot Deinzer |
| Date Deposited: | 02 Sep 2020 06:24 |
| Last Modified: | 02 Sep 2020 06:24 |
| URI: | https://pred.uni-regensburg.de/id/eprint/28158 |
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