This grant announcement from the American Heart Association caught Lab Land’s eye.Â All three of the scientists involved in this project, examining the connections between hypertension, inflammation and the sympathetic nervous system in PTSD, have Emory connections:
*Kerry Ressler, previously Emory Psychiatry/HHMI-supported/Yerkes-based lab/Grady Trauma Project, who moved this summer to Harvard’s McLean Hospital
Related findingÂ that emerged from the Grady Trauma Project: Blood pressure drugs linked with lower PTSD symptoms
*Paul Marvar, who worked with both David Harrison and Kerry Ressler at Emory, and is now at George Washington University
Related item on Marvar’s work: Immune cells required for stress-induced rise in blood pressure in animals
*Jeanie Park, kidney specialist who is here now! The grant is exploring the relationship between the sympathetic nervous system, regulation of blood pressure and PTSD.
2015Â TV interview with Park on her chronic kidney disease research
The connection between stress and blood pressure seems like common sense. Of course experiencing stress — like a narrow miss in morning traffic or dealing with a stubborn, whiny child — raises someoneâ€™s blood pressure.
Try reversing the cause-and-effect relationship: not from brain to body, but instead from body to brain. Could medication for controlling blood pressure moderate the effects of severe stress, and thus aid in controlling PTSD symptoms or in preventing the development of PTSD after trauma?
That was the intriguing implication arising from a 2012 paper from Grady Trauma Project investigators led by psychiatrist Kerry Ressler (lab at Yerkes, supported by HHMI).
They had found that traumatized civilians who take either of two classes of common blood pressure medications tend to have less severe post-traumatic stress symptoms. In particular, individuals taking ACE inhibitors (angiotensin converting enzyme)Â or ARBs (angiotensin receptor blockers)Â tended to have lower levels of hyperarousal and intrusive thoughts, and this effect was not observed with other blood pressure medications.
This was one of those observational findings that needs to be tested in an active way: â€œOK, people who are already taking more X experience less severe symptoms. But can we actually use X as an intervention?â€
In mice, it seems to work. Read more