Angiotensin-II impairs the cellular antioxidant defense capacity in the hypothalamic cardio regulatory nucleus of spontaneously hypertensive rats contributing to hypertension
| Autor: | Andrew Aitken, Francesca Mowry, Sarah Peaden, Vinicia Biancardi |
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| Rok vydání: | 2023 |
| Předmět: | |
| Zdroj: | Physiology. 38 |
| ISSN: | 1548-9221 1548-9213 |
| DOI: | 10.1152/physiol.2023.38.s1.5734703 |
| Popis: | Oxidative stress is a central mechanism underlying Angiotensin II (AngII)-induced enhanced sympathetic outflow within brain cardio-regulatory nuclei in neurogenic hypertension. Yet, a causal association between AngII, Nrf2 (nuclear factor erythroid 2-related factor 2 - the master regulator of the antioxidant response), and sympathetic activity in neurogenic hypertension has not been explored. We hypothesized that increased AngII in neurogenic hypertension impairs the Nrf2 signaling pathway within the paraventricular nucleus of the hypothalamus (PVN), leading to increased oxidative stress, inflammation, and consequent sympathoexcitation. We used 12-13 week-old male hypertensive (SHRs, mean arterial pressure (MAP) 162.8±3.6mmHg; tail-cuff recording [Kent Scientific]) and normotensive Wistar Kyoto rats (WKYs, 107.8±2.1mmHg). We measured mRNA expression in PVN punches (real-time PCR) of the Nrf2 negative regulator Keap1 and Nrf2-based antioxidant defense (Gpx1 and NQO1). We found increased mRNA levels of Keap1 (2.1±0.2) and reductions in Gpx1 (0.7±0.1) and NQO1 (0.5±0.1 fold change) in SHR ( P This work was funded by AHA 953524 to VCB. This is the full abstract presented at the American Physiology Summit 2023 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process. |
| Databáze: | OpenAIRE |
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