ArticleAmerican journal of physiology. Renal physiology2007
Sustained renal interstitial macrophage infiltration following chronic angiotensin II infusions.
Article in American journal of physiology. Renal physiology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 101 papers.
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Who cites it
101 citing papers in PubMed, 146 citations in OpenAlex.
- Salt and chronic kidney disease.Nature reviews. Nephrology · 2026Review
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- The role of M1/M2 macrophage polarization in the pathogenesis of obesity-related kidney disease and related pathologies.Frontiers in immunology · 2024Review
- T-cells regulate albuminuria but not hypertension, renal histology, or the medullary transcriptome in the Dahl SSCD247American journal of physiology. Renal physiology · 2024Article
- Intrarenal renin-angiotensin system activation and macrophage infiltrations in pediatric chronic glomerulonephritis.Pediatric nephrology (Berlin, Germany) · 2023Article
- Depression among Patients with an Implanted Left Ventricular Assist Device: Uncovering Pathophysiological Mechanisms and Implications for Patient Care.International journal of molecular sciences · 2023Review
- Review
- Role of monocytes/macrophages in renin-angiotensin system-induced hypertension and end organ damage.Frontiers in physiology · 2023Review
- Hypertensive Nephropathy: Unveiling the Possible Involvement of Hemichannels and Pannexons.International journal of molecular sciences · 2022Review
- Genetically inducing renal lymphangiogenesis attenuates hypertension in mice.Clinical science (London, England : 1979) · 2022Article
- Immunosuppression by Mycophenolate Mofetil Mitigates Intrarenal Angiotensinogen Augmentation in Angiotensin II-Dependent Hypertension.International journal of molecular sciences · 2022Article
- Effect of Empagliflozin on Sphingolipid Catabolism in Diabetic and Hypertensive Rats.International journal of molecular sciences · 2022Article
- Pathophysiology and genetics of salt-sensitive hypertension.Frontiers in physiology · 2022Review
- The roles of sodium and volume overload on hypertension in chronic kidney disease.Kidney research and clinical practice · 2021Article
- Review
- Amplification of Salt-Sensitive Hypertension and Kidney Damage by Immune Mechanisms.American journal of hypertension · 2021Review
- The Sweet and Salty Dietary Face of Hypertension and Cardiovascular Disease in Lebanon.Frontiers in physiology · 2021Review
- Neurohormones, inflammatory mediators, and cardiovascular injury in the setting of heart failure.Heart failure reviews · 2020Review
- The varying roles of macrophages in kidney injury and repair.Current opinion in nephrology and hypertension · 2020Review
41 more citing papers are in PubMed but not listed here.
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Chronic angiotensin (ANG) II infusions into rats lead to augmented intrarenal levels of ANG II and inflammatory factors, impaired renal function, and progressive hypertension. Residual effects persist after cessation of ANG II infusions, as manifested by a hypertensive response to high-salt intake. This study was performed to determine the residual cytokines and chemokines following the cessation of ANG II infusion. Male Sprague-Dawley rats, maintained on a normal diet, received either a sham operation or continuous ANG II infusion (120 ng/min) subcutaneously via minipumps. The ANG II-infused rats were further subdivided into three subgroups. Minipumps were removed on day 12 with subsequent harvesting of kidneys at 0, 3, and 6 days after cessation of ANG II infusion. After 12 days of ANG II infusion, systolic blood pressure, interstitial fibrosis, preglomerular hypertrophy, and interstitial macrophage infiltration were significantly enhanced compared with the shams. By 3 days following the cessation of ANG II infusion, systolic blood pressure was normalized; however, interstitial fibrosis and preglomerular hypertrophy were still present. Furthermore, increased interstitial macrophage infiltration was still present 6 days after cessation of ANG II infusion. Importantly, augmented mRNA levels of monocyte chemotactic protein (MCP)-1 (1.55 +/- 0.15 vs. 1.00 +/- 0.13, relative ratio) and transforming growth factor (TGF)-beta(1) (1.52 +/- 0.16 vs. 1.00 +/- 0.08) persisted 6 days after the withdrawal of ANG II infusion (1.60 +/- 0.20 for MCP-1 and 1.43 +/- 0.17 for TGF-beta(1)). Thus, the ANG II-induced activation of MCP-1 and TGF-beta(1) is sustained and may account for the persistent effect of chronic ANG II infusions on interstitial macrophage infiltration, suggesting a possible mechanism for the development of salt sensitivity in ANG II-dependent hypertension.
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