| Angiotensin II promotes development of the renal microcirculation through AT1 receptors. | |
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MedLine Citation:
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PMID: 20056745 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Pharmacologic or genetic deletion of components of the renin-angiotensin system leads to postnatal kidney injury, but the roles of these components in kidney development are unknown. To test the hypothesis that angiotensin II supports angiogenesis during postnatal kidney development, we quantified CD31(+) postglomerular microvessels, performed quantitative PCR analysis of vascular growth factor expression, and measured renal blood flow by magnetic resonance. Treating rats with the angiotensin II type 1 receptor antagonist candesartan for 2 weeks after birth reduced the total length, volume, and surface area of capillaries in both the cortex and the medulla and inhibited the organization of vasa recta bundles. In addition, angiotensin II type 1 antagonism inhibited the transcription of angiogenic growth factors vascular endothelial growth factor, angiopoietin-1, angiopoietin-2, and the angiopoietin receptor Tie-2 in cortex and medulla. Similarly, Agtr1a(-/-);Agtr1b(-/-) mouse kidneys had decreased angiopoietin-1, angiopoietin-2, and Tie-2 mRNAs at postnatal day 14. To test whether increased urinary flow leads to microvascular injury, we induced postnatal polyuria with either lithium or adrenalectomy, but these did not alter vascular endothelial growth factor expression or vasa recta organization. Compared with vehicle-treated rats, renal blood flow was significantly (approximately 20%) lower in candesartan-treated rats even 14 days after candesartan withdrawal. Taken together, these data demonstrate that angiotensin II promotes postnatal expansion of postglomerular capillaries and organization of vasa recta bundles, which are necessary for development of normal renal blood flow. |
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Authors:
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Kirsten Madsen; Niels Marcussen; Michael Pedersen; Gitte Kjaersgaard; Carie Facemire; Thomas M Coffman; Boye L Jensen |
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Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't Date: 2010-01-07 |
Journal Detail:
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Title: Journal of the American Society of Nephrology : JASN Volume: 21 ISSN: 1533-3450 ISO Abbreviation: J. Am. Soc. Nephrol. Publication Date: 2010 Mar |
Date Detail:
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Created Date: 2010-03-01 Completed Date: 2010-03-25 Revised Date: 2011-08-03 |
Medline Journal Info:
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Nlm Unique ID: 9013836 Medline TA: J Am Soc Nephrol Country: United States |
Other Details:
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Languages: eng Pagination: 448-59 Citation Subset: IM |
Affiliation:
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Department of Physiology and Pharmacology, University of Southern Denmark, Odense, Denmark. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Adrenalectomy Angiopoietin-1 / analogs & derivatives, genetics Angiopoietin-2 / genetics Angiotensin II / antagonists & inhibitors, metabolism* Angiotensin II Type 1 Receptor Blockers / pharmacology Animals Animals, Newborn Benzimidazoles / pharmacology Capillaries / growth & development*, metabolism Female Kidney / blood supply*, growth & development, pathology Mice Mice, Knockout Neovascularization, Physiologic / drug effects, physiology* Polyuria / pathology, physiopathology RNA, Messenger / metabolism Rats Rats, Sprague-Dawley Receptor, Angiotensin, Type 1 / genetics, metabolism* Receptor, TIE-2 / genetics Renal Circulation / physiology* Tetrazoles / pharmacology Vascular Endothelial Growth Factor A / genetics |
| Chemical | |
Reg. No./Substance:
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0/Angiopoietin-1; 0/Angiopoietin-2; 0/Angiotensin II Type 1 Receptor Blockers; 0/Angpt1 protein, rat; 0/Benzimidazoles; 0/RNA, Messenger; 0/Receptor, Angiotensin, Type 1; 0/Tetrazoles; 0/Vascular Endothelial Growth Factor A; 0/vascular endothelial growth factor A, rat; 11128-99-7/Angiotensin II; 139481-59-7/candesartan; EC 2.7.10.1/Receptor, TIE-2 |
| Comments/Corrections | |
Comment In:
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J Am Soc Nephrol. 2010 Mar;21(3):386-8
[PMID:
20167704
]
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From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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