Propofol and the Renin-Angiotensin System
Abstract
The renin-angiotensin system (RAS) has become a more popular subject of research due to its role in regulating homeostasis within the body as a whole, and regulation of cerebral blood flow, memory consolidation, and etiology of various neurological diseases within the local nervous system RAS. The main effector of the system is Angiotensin (Ang) II, through the activation of the AT1 or AT2 receptor subtypes. Overactivation of the AT1 subtype leads to inflammation and hypertension within the body and an increase in neuronal apoptosis and oxidative stress within the nervous system. Propofol, a commonly used anesthetic in general surgery, has been found to exhibit hypotensive effects and attenuate the results of overactivation of the AT1 receptor by Ang II. A series of competition binding assays have been completed in order to determine if propofol is binding to the AT1 receptor (AT1R) subtype at clinically relevant concentrations in order to exhibit its hypotensive effects and influence AT1R activation by Ang II. This ongoing study has found that propofol does inhibit Ang II binding to the AT1R, however this competition only occurs at high concentrations. This finding implies that the interaction between propofol and the RAS is likely not due to the blocking of the AT1R, rather through another unknown mechanism.
Faculty Sponsors
Dr. Robert Speth
Project Type
Event
Location
Alvin Sherman Library
Start Date
4-6-2021 12:00 PM
End Date
4-9-2021 12:00 PM
Propofol and the Renin-Angiotensin System
Alvin Sherman Library
The renin-angiotensin system (RAS) has become a more popular subject of research due to its role in regulating homeostasis within the body as a whole, and regulation of cerebral blood flow, memory consolidation, and etiology of various neurological diseases within the local nervous system RAS. The main effector of the system is Angiotensin (Ang) II, through the activation of the AT1 or AT2 receptor subtypes. Overactivation of the AT1 subtype leads to inflammation and hypertension within the body and an increase in neuronal apoptosis and oxidative stress within the nervous system. Propofol, a commonly used anesthetic in general surgery, has been found to exhibit hypotensive effects and attenuate the results of overactivation of the AT1 receptor by Ang II. A series of competition binding assays have been completed in order to determine if propofol is binding to the AT1 receptor (AT1R) subtype at clinically relevant concentrations in order to exhibit its hypotensive effects and influence AT1R activation by Ang II. This ongoing study has found that propofol does inhibit Ang II binding to the AT1R, however this competition only occurs at high concentrations. This finding implies that the interaction between propofol and the RAS is likely not due to the blocking of the AT1R, rather through another unknown mechanism.
