ArticleClinical and experimental hypertension (New York, N.Y. : 1993)2014
Vascular oxidative stress upregulates angiotensin II type I receptors via mechanisms involving nuclear factor kappa B.
Article in Clinical and experimental hypertension (New York, N.Y. : 1993), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 38 citations in OpenAlex.
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- Oxidative Stress in Kidney Injury and Hypertension.Antioxidants (Basel, Switzerland) · 2024Review
- Aging and "Age-Related" Diseases - What Is the Relation?Aging and disease · 2024Review
- Alpha-lipoic acid: A promising pharmacotherapy seen through the lens of kidney diseases.Current research in pharmacology and drug discovery · 2024Review
- Iron chelation suppresses secondary bleeding after intracerebral hemorrhage in angiotensin II-infused mice.CNS neuroscience & therapeutics · 2021Article
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- Antioxidant Effects of PS5, a Peptidomimetic of Suppressor of Cytokine Signaling 1, in Experimental Atherosclerosis.Antioxidants (Basel, Switzerland) · 2020Article
- The natural drug DIAVIT is protective in a type II mouse model of diabetic nephropathy.PloS one · 2019Article
- Dysregulation of the Renin-Angiotensin System and the Vasopressinergic System Interactions in Cardiovascular Disorders.Current hypertension reports · 2018Review
- Vascular Oxidative Stress: Impact and Therapeutic Approaches.Frontiers in physiology · 2018Review
- Article
- Endoplasmic reticulum stress increases AT1R mRNA expression via TIA-1-dependent mechanism.Nucleic acids research · 2016Article
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- Angiotensin-(1-7) counteracts the effects of Ang II on vascular smooth muscle cells, vascular remodeling and hemorrhagic stroke: Role of the NFкB inflammatory pathway.Vascular pharmacology · 2015Article
- Chronic NF-κB blockade improves renal angiotensin II type 1 receptor functions and reduces blood pressure in Zucker diabetic rats.Cardiovascular diabetology · 2015Article
- Beneficial effects of ethanol extracts of Red Liriope platyphylla on vascular dysfunction in the aorta of spontaneously hypertensive rats.Laboratory animal research · 2015Article
- The protective effect of lipoic acid on selected cardiovascular diseases caused by age-related oxidative stress.Oxidative medicine and cellular longevity · 2015Review
- Anti-hypertensive Herbs and their Mechanisms of Action: Part I.Frontiers in pharmacology · 2015Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
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Abstract
Abstract The association of oxidative stress with hypertension is well known. However, a causal role of oxidative stress in hypertension is unclear. Vascular angiotensin II type 1 receptor (AT1R) upregulation is a prominent contributor to pathogenesis of hypertension. However, the mechanisms causing this upregulation are unknown. Oxidative stress is an important regulator of protein expression via activation of transcription factors such as nuclear factor kappa B (NFκB). The present study was carried out to test the hypothesis that oxidative stress contributes to vascular AT1R upregulation via NFκB in human aortic smooth muscle cells (HASMC) and spontaneously hypertensive rats (SHR). HASMC exposed to oxidative stress exhibited a robust increase in AT1R mRNA in HASMC. Furthermore, oxidative stress failed to upregulate AT1Rs in the presence of either an antioxidant catalase or siRNA against p65 subunit of NFκB. To test the role of oxidative stress and NFκB in hypertension, prehypertensive SHR were treated with NFκB inhibitor pyrrolidine dithiocarbamate from 5 weeks to 11-12 weeks of age. At 11-12 weeks of age, SHR exhibited increased NFκB expression, AT1R upregulation and exaggerated Ang II-induced vasoconstriction as compared to age-matched Wistar Kyoto (WKY) rats. PDTC treatment of SHR lowered NFκB expression, normalized AT1R expression and Ang II-induced vasoconstriction. More importantly, PDTC treatment significantly attenuated hypertension development in SHR. In conclusion, vascular oxidative can upregulate AT1R, via mechanisms involving NFκB, and contribute to the development of hypertension.
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