CNS neuroplasticity and salt-sensitive hypertension induced by prior treatment with subpressor doses of ANG II or aldosterone

Sarah C. Clayton, Zhongming Zhang, Terry Beltz, Baojian Xue, and Alan Kim Johnson.

Am J Physiol Regul Integr Comp Physiol 306: R908–R917, 2014.First published April 2, 2014; doi:10.1152/ajpregu.00010.2014. Hypertension is obviously a problem in today’s society.  About 25% of all hypertensive patients are salt sensitive. However the mechanism that is responsible for salt sensitivity leading to hypertension is still not clearly understood. It has been shown that pretreatment with  nonpressor doses of ANG II and aldosterone can lead to enhanced responses to ANG II. This sensitization depends on a functional brain renin angiotensin aldosterone system. Long term changes in the CNS could occur in response to sensitization. This studied investigated whether BDNF a protein that plays a role in many models neuroplasticity is involved in the changes that are occurring in the lamina terminalis (LT) in response to sensitization to ANGII.  the study showed that pretreatment to ANGII or Aldosterone in the brain can lead sensitization to salt. They also showed that the BDNF is enhanced along with p38 MARK and pCREB in response to pretreatment to ANGII and aldosterone. These data demonstrate that pretreatment with subpressor doses of ANGII and aldosterone can lead long term structural changes by increasing the the BDNF pathway in LT and this contributes to the development of salt sensitivity. I wished they would have investigated the RVLM, wouldn’t that be interesting.-MD