Lesion of the commissural nucleus of the solitary tract/A2 noradrenergic neurons facilitates the activation of angiotensinergic mechanisms in response to hemorrhage.

Neuroscience. 2013 Dec 19;254:196-204. doi: 10.1016/j.neuroscience.2013.09.017. Epub 2013 Sep 20. Freiria-Oliveira AH1, Blanch GT, De Paula PM, Menani JV, Colombari DS. I'll be honest, I chose this week's papers based on the fact that they came from the lab of my EB2014 meeting mentor, Débora Colombari. I was not very familiar with the work from this lab before EB, but it turns out they work on the NTS and AT1, which is something our lab has talked about on a number of occasions. In this paper, they used anti-dbh-sapporin to lesion the noradrenergic cells in the NTS, a.k.a the A2 group. They then induced a pretty heavy 4-step hemorrhage in rats and looked at the how a lack of the A2 group affects blood pressure. If you're curious about the proximity of the RVLM to the NTS and if their lesions might have affected the C1 neurons (which was my first thought), their first figure in the paper shows that while the NTS had a huge reduction in TH-positive cells, the RVLM appeared to be in perfect shape. Anyway, what they found was that lesioned rats actually recovered their blood pressure FASTER than control rats after hemmorhage, and that application of losartan (iv or intracerebroventricular) could block this change. Their argument is that A2 neurons probably work to inhibit angiotensinergic pathways. I don't claim to know all the neural microcircuitry, but since we're an RVLM lab... maybe we can claim that it's all because of NTS-CVLM-RVLM-RSNA? -DH