ArticleAmerican journal of physiology. Regulatory, integrative and comparative physiology2009
Angiotensin II AT1 blockade reduces the lipopolysaccharide-induced innate immune response in rat spleen.
Article in American journal of physiology. Regulatory, integrative and comparative physiology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 46 citations in OpenAlex.
- Angiotensin II Receptor Signaling in the Hypothalamic-Pituitary-Adrenal Axis and Spleen After Spinal Cord Injury Depends on the Sympathetic Innervation Integrity.Cellular and molecular neurobiology · 2026Article
- The therapeutic potential of losartan in lung metastasis of colorectal cancer.EXCLI journal · 2020Article
- Fimasartan reduces neointimal formation and inflammation after carotid arterial injury in apolipoprotein E knockout mice.Molecular medicine (Cambridge, Mass.) · 2019Article
- Repeated Stress Exaggerates Lipopolysaccharide-Induced Inflammatory Response in the Rat Spleen.Cellular and molecular neurobiology · 2018Article
- SGK1-FoxO1 Signaling Pathway Mediates Th17/Treg Imbalance and Target Organ Inflammation in Angiotensin II-Induced Hypertension.Frontiers in physiology · 2018Article
- The weakening effect of soluble epoxide hydrolase inhibitor AUDA on febrile response to lipopolysaccharide and turpentine in rat.Journal of physiology and biochemistry · 2017Article
- The renin-angiotensin system: a possible new target for depression.BMC medicine · 2017Review
- The angiotensin receptor blocker, Losartan, inhibits mammary tumor development and progression to invasive carcinoma.Oncotarget · 2017Article
- Angiotensin II type-1 receptor (ATScientific reports · 2016Article
- Article
- The immune system and hypertension.Immunologic research · 2014Review
- The immune system in hypertension.Advances in physiology education · 2014Review
- Article
- Angiotensin II AT(1) receptor blockers as treatments for inflammatory brain disorders.Clinical science (London, England : 1979) · 2012Review
- Neurohormonal modulation of the innate immune system is proinflammatory in the prehypertensive spontaneously hypertensive rat, a genetic model of essential hypertension.Circulation research · 2012Article
- Angiotensin II AT(1) receptor blockers ameliorate inflammatory stress: a beneficial effect for the treatment of brain disorders.Cellular and molecular neurobiology · 2012Review
- Adiponectin and plant-derived mammalian adiponectin homolog exert a protective effect in murine colitis.Digestive diseases and sciences · 2011Article
- Epigallocatechin-3-gallate Regulates Inducible Nitric Oxide Synthase Expression in Human Umbilical Vein Endothelial Cells.Laboratory animal research · 2011Article
- Angiotensin II AT1 receptor blockade ameliorates brain inflammation.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2011Article
- Blockade of brain angiotensin II AT1 receptors ameliorates stress, anxiety, brain inflammation and ischemia: Therapeutic implications.Psychoneuroendocrinology · 2011Review
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8 authors at 1 institution in 1 country.
Funding
Abstract
ANG II AT(1) receptor blockade reduces inflammation in hypertension. To determine whether ANG II AT(1) receptor blockers (ARBs) influence the innate immune inflammatory response in normotensive rats, we studied rat plasma and spleen after a 3-day subcutaneous pretreatment with the ARB candesartan followed by a single dose of the bacterial endotoxin LPS (50 microg/kg ip). Peripheral administration of LPS to rodents produced a generalized inflammatory response with increased release of TNF-alpha, IL-1beta, and IL-6 into the circulation. Candesartan pretreatment reduced the LPS-induced release of TNF-alpha, IL-1beta, and IL-6 into the circulation. The red pulp of rat spleen expressed large numbers of AT(1) receptors and the LPS receptors Toll-like receptor 4 and CD14. Candesartan administration significantly blocked AT(1) receptors. The ARB reduced the LPS-induced upregulation of CD14 gene expression; expression of TNF-alpha and IL-6 mRNA and protein; expression of IL-1beta and IkappaB-alpha mRNA; COX-2 mRNA and protein expression and PGE(2) concentration; inducible nitric oxide synthase (iNOS) gene and protein expression and iNOS activity; and Nox2 gene expression and 8-isoprostane levels. In addition, candesartan reduced the CD14 protein expression in saline- and LPS-treated rats. Our results suggest that AT(1) receptors are essential for the development of the full innate immune response to bacterial endotoxin. The ARB decreased the general peripheral inflammatory reaction to LPS and partially decreased the inflammatory response in the spleen. An unrestricted innate immune response to the bacterial endotoxin may have deleterious effects for the organism and may lead to development of chronic inflammatory disease. We postulate that ARBs may have therapeutic effects on inflammatory conditions.
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