ArticleAmerican journal of physiology. Renal physiology2011
Renal injury in angiotensin II+L-NAME-induced hypertensive rats is independent of elevated blood pressure.
Article in American journal of physiology. Renal physiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 27 citations in OpenAlex.
- UNI-494 treatment improves measures of renal dysfunction and cardiac pathology in male rats receiving L-NAME and angiotensin II.Physiological reports · 2025Article
- Renoprotective effects of compound 21 and empagliflozin in L-Name-induced hypertensive rats.BMC urology · 2025Article
- Brown-Norway chromosome 1 mitigates the upregulation of proinflammatory pathways in mTAL cells and subsequent age-related CKD in Dahl SS/JrHsdMcwi rats.American journal of physiology. Renal physiology · 2023Article
- Acute Increase of Renal Perfusion Pressure Causes Rapid Activation of mTORC1 (Mechanistic Target Of Rapamycin Complex 1) and Leukocyte Infiltration.Hypertension (Dallas, Tex. : 1979) · 2022Article
- Renal Perfusion Pressure Determines Infiltration of Leukocytes in the Kidney of Rats With Angiotensin II-Induced Hypertension.Hypertension (Dallas, Tex. : 1979) · 2020Article
- Ivabradine Ameliorates Kidney Fibrosis in L-NAME-Induced Hypertension.Frontiers in medicine · 2020Article
- The Effects of Irisin on Nω-Nitro-L-arginine Methyl Ester Hydrochloride-Induced Hypertension in RatsBalkan medical journal · 2019Article
- Transcriptomic analysis reveals inflammatory and metabolic pathways that are regulated by renal perfusion pressure in the outer medulla of Dahl-S rats.Physiological genomics · 2018Article
- Increased Perfusion Pressure Drives Renal T-Cell Infiltration in the Dahl Salt-Sensitive Rat.Hypertension (Dallas, Tex. : 1979) · 2017Article
- The cooperative roles of inflammation and oxidative stress in the pathogenesis of hypertension.Antioxidants & redox signaling · 2014Review
- Early life stress induces renal dysfunction in adult male rats but not female rats.American journal of physiology. Regulatory, integrative and comparative physiology · 2013Article
- Effect of P2X4 and P2X7 receptor antagonism on the pressure diuresis relationship in rats.Frontiers in physiology · 2013Article
- Lack of specificity of commercial antibodies leads to misidentification of angiotensin type 1 receptor protein.Hypertension (Dallas, Tex. : 1979) · 2013Article
- Contribution of cytochrome P450 1B1 to hypertension and associated pathophysiology: a novel target for antihypertensive agents.Prostaglandins & other lipid mediators · 2012Review
- Increased susceptibility to kidney injury by transfer of genomic segment from SHR onto Dahl S genetic background.Physiological genomics · 2012Article
- Involvement of cytochrome P-450 1B1 in renal dysfunction, injury, and inflammation associated with angiotensin II-induced hypertension in rats.American journal of physiology. Renal physiology · 2012Article
- Cytochrome P450 1B1 contributes to renal dysfunction and damage caused by angiotensin II in mice.Hypertension (Dallas, Tex. : 1979) · 2012Article
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3 authors at 1 institution in 1 country.
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Abstract
The balance between angiotensin II (ANG II) and nitric oxide plays an important role in renal function and is thought to contribute to the progression of renal injury in experimental hypertension. In the present study, we investigated the extent of blood pressure (BP)-dependent and BP-independent pathways of renal injury following 2 wk of hypertension produced by intravenous infusion of ANG II (5 ng·kg⁻¹·min⁻¹)+N(ω)-nitro-l-arginine methyl ester (l-NAME; 1.4 μg·kg⁻¹·min⁻¹) in male Sprague-Dawley rats. An aortic balloon occluder was positioned between the renal arteries to maintain (24 h/day) BP to the left kidney (servo-controlled) at baseline levels, whereas the right kidney (uncontrolled) was chronically exposed to elevated BP. Over the 14-day experimental protocol, the average BP to uncontrolled kidneys (152.7 ± 1.8 mmHg) was significantly elevated compared with servo-controlled (113.0 ± 0.2 mmHg) kidneys and kidneys from sham rats (108.3 ± 0.1 mmHg). ANG II+l-NAME infusion led to renal injury that was focal in nature and mainly confined to the outer medulla. Despite the differences in BP between servo-controlled and uncontrolled kidneys, there was a similar ~3.5-fold increase in renal outer medullary tubular injury, ~2-fold increase in outer medullary interstitial fibrosis, ~2-fold increase in outer medullary macrophage infiltration, and a significant increase in renal oxidative stress, all of which are indicative of BP-independent mediated pathways. The results of this study have important implications regarding the pathogenesis of renal injury in various experimental models of hypertension and provide novel insights regarding the variable association observed between hypertension and renal injury in some human populations.
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