Glutamatergic Receptor Activation in the Rostral Ventrolateral Medulla Mediates the Sympathoexcitatory Response to Hyperinsulinemia

Megan E. Bardgett, John J. McCarthy and Sean D. Stocker Hypertension. 2010;55:284-290; originally published online January 11, 2010; doi: 10.1161/HYPERTENSIONAHA.109.146605 We know that in rodent models of obesity it has been shown that there is elevated sympathetic nervous system activity. This article investigated whether this was due to increased glutametergic input to rvlm or some other type of excitatory input. In response glucose infusion, low fat diet and obese resistant rats had lower in plasma levels of insulin when compared to obesity prone rats. In animals that were hyperinsulinemic kyn injections into rvlm lead to caused lumber sna to increase but not arterial pressure. They injected AP5 into rvlm in irder to block NMDA receptors and showed that there was a drop in bp similar to the kyn response. They also gave NBQX and saw no effect on lsna an ABP. They also blocked AT1 and melanocortin receptors and found that it had no effect on sympathoexcitatory responses. They did western blot in order to look at insulin receptor expression in the RVLM they found that there was essentially no insulin receptor present. Also when they injected insulin into the RVLM it did not alter lsna and ABP. These data suggest that the elevated sympathetic nerve activity that is seen in metabolic syndromes is most likely due to enhanced glutamergic receptor activation.-MD