ArticleBritish journal of pharmacology2000
Negative feedback regulation of reactive oxygen species on AT1 receptor gene expression.
Article in British journal of pharmacology, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 56 citations in OpenAlex.
- Aerobic Exercise Training Reduces Atherogenesis Induced by Low-Sodium Diet in LDL Receptor Knockout Mice.Antioxidants (Basel, Switzerland) · 2022Article
- Sensitization of the Angiotensin II AT1 Receptor Contributes to RKIP-Induced Symptoms of Heart Failure.Frontiers in medicine · 2018Article
- Low-sodium diet induces atherogenesis regardless of lowering blood pressure in hypertensive hyperlipidemic mice.PloS one · 2017Article
- Binding of EBP50 to Nox organizing subunit p47phox is pivotal to cellular reactive species generation and altered vascular phenotype.Proceedings of the National Academy of Sciences of the United States of America · 2016Article
- International Union of Basic and Clinical Pharmacology. XCIX. Angiotensin Receptors: Interpreters of Pathophysiological Angiotensinergic Stimuli [corrected].Pharmacological reviews · 2015Review
- Cardiovascular-renal and metabolic characterization of a rat model of polycystic ovary syndrome.Gender medicine · 2011Article
- Oxidative Stress and Vascular Damage in Hypertension: Role of Angiotensin II.International journal of hypertension · 2011Article
- Neonatal intermittent hypoxia impairs neuronal nicotinic receptor expression and function in adrenal chromaffin cells.American journal of physiology. Cell physiology · 2010Article
- Expression of angiotensin II receptor type 1 is reduced in advanced rat liver fibrosis.Digestive diseases and sciences · 2007Article
- New insights on receptor-dependent and monoamine oxidase-dependent effects of serotonin in the heart.Journal of neural transmission (Vienna, Austria : 1996) · 2007Review
- Effects of various oxidants and antioxidants on the p38-MAPK signalling pathway in the perfused amphibian heart.Molecular and cellular biochemistry · 2006Article
- Reactive oxygen species in vascular biology: implications in hypertension.Histochemistry and cell biology · 2004Review
- Hypertension and lipids: lipid factors in the hypertension syndrome.Current hypertension reports · 2002Review
- Central role of the AT(1)-receptor in atherosclerosis.Journal of human hypertension · 2002Review
- Reactive oxygen species: roles in blood pressure and kidney function.Current hypertension reports · 2002Review
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Free radicals as well as the AT1 receptor are involved in the pathogenesis of cardiovascular disease. Both the intracellular mechanisms of AT1 receptor regulation and the effect of free radicals on AT1 receptor expression are currently unknown. This study investigates the role of free radicals in the modulation of AT1 receptor expression and in the angiotensin II-induced AT1 receptor regulation. AT1 receptor mRNA was assessed by Northern blotting and AT1 receptor density by radioligand binding assays, respectively, in vascular smooth muscle cells (VSMC). Free radical release was measured by confocal laser scanning microscopy. AT1 receptor mRNA transcription rate was determined by nuclear run-on assays and AT1 receptor mRNA half-life was measured under transcriptional blockade. Angiotensin II caused a time-dependent decrease of AT1 receptor mRNA expression in rat VSMC in culture (30+/-6% at 4 h with 100 nM angiotensin II). This was followed by a consistent decrease in AT1 receptor density. Angiotensin II caused release of reactive oxygen species in VSMC which was abolished by preincubation with 100 microM diphenylene iodonium (DPI). DPI inhibited partially the down-regulating effect of angiotensin II on the AT1 receptor. Incubation of VSMC with either hydrogen peroxide or xanthine/xanthine oxidase caused a dose-dependent decrease in AT1 receptor mRNA expression which was not mediated by a decreased rate of transcription but rather through destabilization of AT1 receptor mRNA. Experiments which included preincubation of VSMC with various intracellular inhibitors suggested that free radicals caused AT1 receptor downregulation through activation of p38-MAP kinase and intracellular release of calcium. However, angiotensin II-induced AT1 receptor expression was not inhibited by blockade of p38-MAP kinase activation or intracellular calcium release. Free radicals may at least in part mediate angiotensin II-induced AT1 receptor regulation through direct post-transcriptional effects on AT1 receptor mRNA expression which involves intracellular release of calcium and activation of p38-MAP kinase. These findings may help to clarify the intracellular mechanisms involved in AT1 receptor regulation and reveal a novel biological feature for reactive oxygen species.
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