NDLI: Intrarenal angiotensin II and angiotensinogen augmentation in chronic angiotensin II-infused mice.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Gonzalez-Villalobos, Romer A. Seth, Dale M. Satou, Ryousuke Horton, Heather Ohashi, Naro Miyata, Kayoko Katsurada, Akemi Tran, Duy V. Kobori, Hiroyuki Navar, L. G.
Description	Country affiliation: United States Author Affiliation: Gonzalez-Villalobos RA ( Department of Physiology, Tulane University Health Sciences Center, 1430 Tulane Avenue, New Orleans, LA 70112, USA. rgonzale@tulane.edu)
Abstract	The objectives of this study were to determine the effects of chronic angiotensin II (ANG II) infusions on ANG II content and angiotensinogen expression in the mouse kidney and the role of the angiotensin II type 1 receptor (AT(1)R) in mediating these changes. C57BL/6J male mice were subjected to ANG II infusions at doses of 400 or 1,000 ng.kg(-1).min(-1) either alone or with an AT(1)R blocker (olmesartan; 3 mg.kg(-1).day(-1)) for 12 days. Systolic and mean arterial pressures were determined by tail-cuff plethysmography and radiotelemetry. On day 13, blood and kidneys were collected for ANG II determinations by radioimmunoanalysis and intrarenal angiotensinogen expression studies by quantitative RT-PCR, Western blotting, and immunohistochemistry. ANG II infusions at the low dose elicited progressive increases in systolic blood pressure (135 +/- 2.5 mmHg). In contrast, the high dose induced a rapid increase (152 +/- 2.5, P < 0.05 vs. controls, 109 +/- 2.8). Renal ANG II content was increased by ANG II infusions at the low dose (1,203 +/- 253 fmol/g) and the high dose (1,258 +/- 173) vs. controls (499 +/- 40, P < 0.05). Kidney angiotensinogen mRNA and protein were increased only by the low dose to 1.13 +/- 0.02 and 1.26 +/- 0.10, respectively, over controls (1.00, P < 0.05). These effects were not observed in mice infused at the high dose and those receiving olmesartan. The results indicate that chronic ANG II infusions augment mouse intrarenal ANG II content with AT(1)R-dependent uptake occurring at both doses, but only the low dose of infusion, which elicited a slow progressive response, causes an AT(1)R-dependent increase in intrarenal angiotensinogen expression.
File Format	HTM / HTML
ISSN	1931857X
e-ISSN	15221466
DOI	10.1152/ajprenal.00019.2008
Journal	AJP: Renal Physiology
Issue Number	3
Volume Number	295
Language	English
Publisher	American Physiological Society
Publisher Date	2008-09-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Hypertension Receptor, Angiotensin, Type 1 Blood Pressure Research Support, N.i.h., Extramural Research Support, Non-u.s. Gov't Body Weight Mice, Inbred C57bl Organ Size Discipline Nephrology Administration & Dosage Metabolism Kidney Blood Chemically Induced Discipline Physiology Pathology Animals Renin Angiotensinogen Mice Angiotensin Ii
Content Type	Text
Resource Type	Article
Subject	Physiology Urology

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