Neurons in the Organum Vasculosum of the Lamina Terminalis Sense Both Angiotensin II and NaCl to Regulate Thirst

2018 ◽  
Vol 32 (S1) ◽  
Author(s):  
Brian J. Kinsman ◽  
Kirsteen N. Browning ◽  
Sean D. Stocker
Keyword(s):  
Angiotensin Ii ◽  
Lamina Terminalis ◽  
Organum Vasculosum

scholarly journals Integration of Hypernatremia and Angiotensin II by the Organum Vasculosum of the Lamina Terminalis Regulates Thirst

2020 ◽  
Vol 40 (10) ◽  
pp. 2069-2079
Author(s):  
Brian J. Kinsman ◽  
Sarah S. Simmonds ◽  
Kirsteen N. Browning ◽  
Megan M. Wenner ◽  
William B. Farquhar ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Lamina Terminalis ◽  
Organum Vasculosum

scholarly journals Angiotensin II-Induced Hypertension Is Attenuated by Overexpressing Copper/Zinc Superoxide Dismutase in the Brain Organum Vasculosum of the Lamina Terminalis

2016 ◽  
Vol 2016 ◽  
pp. 1-9 ◽  
Author(s):  
John P. Collister ◽  
Heather Taylor-Smith ◽  
Donna Drebes ◽  
David Nahey ◽  
Jun Tian ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Superoxide Dismutase ◽  
Angiotensin Ii ◽  
Intracellular Signaling ◽  
Lamina Terminalis ◽  
Copper Zinc Superoxide Dismutase ◽  
Zinc Superoxide Dismutase ◽  
Copper Zinc ◽  
Organum Vasculosum ◽  
The Brain

Angiotensin II (AngII) can access the brain via circumventricular organs (CVOs), including the subfornical organ (SFO) and organum vasculosum of the lamina terminalis (OVLT), to modulate blood pressure. Previous studies have demonstrated a role for both the SFO and OVLT in the hypertensive response to chronic AngII, yet it is unclear which intracellular signaling pathways are involved in this response. Overexpression of copper/zinc superoxide dismutase (CuZnSOD) in the SFO has been shown to attenuate the chronic hypertensive effects of AngII. Presently, we tested the hypothesis that elevated levels of superoxide (O2∙-) in the OVLT contribute to the hypertensive effects of AngII. To facilitate overexpression of superoxide dismutase, adenoviral vectors encoding human CuZnSOD or control adenovirus (AdEmpty) were injected directly into the OVLT of rats. Following 3 days of control saline infusion, rats were intravenously infused with AngII (10 ng/kg/min) for ten days. Blood pressure increased33±8 mmHg in AdEmpty rats (n=6), while rats overexpressing CuZnSOD (n=8) in the OVLT demonstrated a blood pressure increase of only18±5 mmHg after 10 days of AngII infusion. These results support the hypothesis that overproduction ofO2∙-in the OVLT plays an important role in the development of chronic AngII-dependent hypertension.

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