Discharge of RVLM vasomotor neurons is not increased in anesthetized angiotensin II-salt hypertensive rats.

Pedrino GR, Calderon AS, Andrade MA, Cravo SL, Toney GM. Am J Physiol Heart Circ Physiol. 2013 Dec;305(12):H1781-9. I might get in trouble for saying this... but I kind of dislike this paper for personal reasons. These people are also interested in differences in RVLM neuron firing rates between normotensive and hypertensive rats. They looked at the difference in RVLM unit activity between normotensive (NT) rats and rats that had become hypertensive (HT) due to three weeks of AngII infusion and consumption of a high-salt diet. Neurons were confirmed to be presympathetic and spinally projecting via baroinhibition and antidromic action potentials. They noted that the neurons fired one spike per heart beat, which was likely to fire during mid-late systole, which was not different between groups. The discharge rate at resting MAP was similar between groups, so they looked at barosensitivity and found that HT rats required a higher increase in MAP before they would stop firing. They also used nitroprusside to unload baroreceptors and found that both groups had similar maximum discharge rates and requisite change in MAP needed to achieve these max rates, but within a certain range of MAPs (120-150mmHg) neurons in HT rats were more likely to be firing at a higher rate. This says that just like we would expect to see in our exercise vs inactivity model, unhealthy rats are reluctant to decrease a high sympathetic tone even when there is no physiologic need for it. They also did juxtacellular of some cells found that in NT rats, 3 were C1 (PNMT positive) and 4 were non-C1. In HT rats, 6 were C1 and 6 were non-C1. -DH