ArticleAmerican journal of physiology. Renal physiology2016
Increased angiotensinogen expression, urinary angiotensinogen excretion, and tissue injury in nonclipped kidneys of two-kidney, one-clip hypertensive rats.
Article in American journal of physiology. Renal physiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 15 citations in OpenAlex.
- Early-stage 2K1C renovascular hypertension does not increase global MHC-II or F4/80 abundance in the non-clipped kidney but reveals focal F4/80Experimental physiology · 2026Article
- (Pro)renin Receptor Blockade Prevents Increases in Systolic Blood Pressure, Sodium Retention, and αENaC Protein Expression in the Kidney of 2K1C Goldblatt Mice.International journal of molecular sciences · 2025Article
- Solitary Functioning Kidneys Attenuate Renal Hemodynamics Responses to Angiotensin II in Male But Not in Female Rats.International journal of preventive medicine · 2024Article
- Genetic Deletion of ATInternational journal of molecular sciences · 2022Article
- Immunosuppression by Mycophenolate Mofetil Mitigates Intrarenal Angiotensinogen Augmentation in Angiotensin II-Dependent Hypertension.International journal of molecular sciences · 2022Article
- Article
- Mutagenesis of the Cleavage Site of Pro Renin Receptor Abrogates Angiotensin II-Induced Hypertension in Mice.Hypertension (Dallas, Tex. : 1979) · 2021Article
- Sex Differences in the Renal Vascular Responses of ATInternational journal of hypertension · 2021Article
- Sex dimorphism in ANGII-mediated crosstalk between ACE2 and ACE in diabetic nephropathy.Laboratory investigation; a journal of technical methods and pathology · 2018Article
- Is angiotensin-(3-4) (Val-Tyr), the shortest angiotensin II-derived peptide, opening new vistas on the renin-angiotensin system?Journal of the renin-angiotensin-aldosterone system : JRAAS · 2017Review
- Renal disease pathophysiology and treatment: contributions from the rat.Disease models & mechanisms · 2016Review
- Article
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
Abstract
In angiotensin II (ANG II)-dependent hypertension, there is an angiotensin type 1 receptor-dependent amplification mechanism enhancing intrarenal angiotensinogen (AGT) formation and secretion in the tubular fluid. To evaluate the role of increased arterial pressure, AGT mRNA, protein expression, and urinary AGT (uAGT) excretion and tissue injury were assessed in both kidneys of two-kidney, one-clip Sprague-Dawley hypertensive rats subjected to left renal arterial clipping (0.25-mm gap). By 18-21 days, systolic arterial pressure increased to 180 ± 3 mmHg, and uAGT increased. Water intake, body weights, 24-h urine volumes, and sodium excretion were similar. In separate measurements of renal function in anesthetized rats, renal plasma flow and glomerular filtration rate were similar in clipped and nonclipped kidneys and not different from those in sham rats, indicating that the perfusion pressure to the clipped kidneys remained within the autoregulatory range. The nonclipped kidneys exhibited increased urine flow and sodium excretion. The uAGT excretion was significantly greater in nonclipped kidneys compared with clipped and sham kidneys. AGT mRNA was 2.15-fold greater in the nonclipped kidneys compared with sham (1.0 ± 0.1) or clipped (0.98 ± 0.15) kidneys. AGT protein levels were also greater in the nonclipped kidneys. The nonclipped kidneys exhibited greater glomerular expansion and immune cell infiltration, medullary fibrosis, and cellular proliferation than the clipped kidneys. Because both kidneys have elevated ANG II levels, the greater tissue injury in the nonclipped kidneys indicates that an increased arterial pressure synergizes with increased intrarenal ANG II to stimulate AGT production and exert greater renal injury.
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