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The Role Of Central Ace2 And Nrf2 In Sympatho-Excitation: Responses To Central Angiotensin Ii, Anyun Ma May 2020

The Role Of Central Ace2 And Nrf2 In Sympatho-Excitation: Responses To Central Angiotensin Ii, Anyun Ma

Theses & Dissertations

Sympatho-excitation is a key characteristic in cardiovascular diseases such as chronic heart failure (CHF) and primary Hypertension (HTN). Evidence suggests that increased sympathetic tone is closely related to activation of the Renin-Angiotensin-Aldosterone system (RAAS) in the central nervous system. An underlying mechanism for sympatho-excitation is thought to be oxidative stress resulting from Angiotensin II (AngII) type 1 receptor (AT1R) activation. Over the past several decades, pharmacological targeting of components of the RAAS have been used as standard therapy in CHF and HTN. However, additional therapeutic strategies are necessary to control these diseases. Oxidative stress is regulated, in part, by the …


Role Of Redox-Sensitive Calcium/Calmodulin-Dependent Protein Kinase Lla In Angiotensin Ii Intra-Neuronal Signaling And Angiotensin Ll-Mediated Hypertension, Urmi Basu Aug 2015

Role Of Redox-Sensitive Calcium/Calmodulin-Dependent Protein Kinase Lla In Angiotensin Ii Intra-Neuronal Signaling And Angiotensin Ll-Mediated Hypertension, Urmi Basu

Theses & Dissertations

Activation of renin-angiotensin system and elevated levels of circulating and brain angiotensin II (AngII) has been implicated in the pathogenesis of neuro-cardiovascular diseases, such as hypertension and heart failure. In central neurons AngII increases generation of reactive oxygen species (ROS), which in turn regulates neuronal ion channels. Previous studies have demonstrated that ion channels can also be regulated by protein kinases, such as calcium /calmodulin-dependent protein kinase II (CaMKII) as a downstream mediator of AngII signaling. In the heart, CaMKIIδ undergoes oxidation upon AngII stimulation and increased pro-oxidant conditions. However, the exact mechanism by which AngII and ROS regulate CaMKIIα, …