Lesions in Rostral Ventromedial or RVLM Block Neurogenic Hypertension

by Kurt J. Varner, Elisardo C. Vasquez and Michael J. Brody

This study used NMDA-induced lesions of the RVLM or RVMM to determine whether neurons in either region are involved in the acute hypertension and tachycardia produced by sinoaortic deafferentiation (SAD). SAD is a technique used to induce hypertension by surgically interrupting peripheral baroreceptor afferent nerves.

First, NMDA was injected into the RVLM and RVMM. As the name would suggest, NMDA binds to NMDA-receptors, which are the glutamatergic receptors on neurons in the RVLM. However, NMDA does not have the same excitatory effects that glutamate does. Instead, it is an excitotoxin which means that it kills neurons by overexciting them. Following NMDA-lesion, SAD was performed. There were 4 groups used in this experiment: sham lesion (saline injection into RVLM or RVMM), NMDA lesion (lesion of sites rostral to RVLM or RVMM), RVLM lesion and RVMM lesion.

MAP decreased in both RVLM and RVMM conditions. RVLM lesioned animals showed the lowest MAP in both post-lesion and post-lesion + SAD conditions. The lack of hypertensive response likely reflects the loss of baroreceptor-sensitive sympathoexcitatory neurons in these regions. This study shows that both the RVLM and RVMM are involved in the development of neurogenic hypertension under these conditions.

-BH