Tonic glutamate-mediated control of rostral ventrolateral medulla and sympathetic vasomotor tone.

Ito S, Sved AF.
Am J Physiol. 1997 Aug;273(2 Pt 2):R487-94.

Previously studies by Guyenet et al., showed that when glutamate receptors are blocked bilaterally in the RVLM using kynurenic acid (glutamate receptor antagonist) it produced no significant changes in the arterial pressure suggesting that glutamate may not play a role in tonic activation of RVLM pre-sympathetic neurons. In this article the authors questioned this notion. The authors hypothesized that if CVLM-mediated inhibition of RVLM is removed then excitatory amino acids (EAA) could provide neuronal excitation and in turn an increase in arterial pressure. Male Sprague-Dawely rats were used for this study. Two different types of anesthesia were used in this experiment, alpha-chloralose or urethane both given intravenously to show that changes seen were not specific to anesthetic that is used. The major finding of the present study is that when CVLM was inhibited by micro injection of muscimol (GABA-A receptor agonist), it markedly increased the arterial pressure, subsequently when kynurenic acid (kyn) was injected into the RVLM it decreased the elevated arterial pressure. Interestingly when only kyn was injected it produced mild changes in the arterial pressure. These findings show that the when CVLM was inhibited it increased arterial pressure and this could be mediated through RVLM neurons excited by EAA. One possible explanation for this results is that on one hand the glutamatergic inputs to the RVLM are excited to activate the sympathoexcitatory neurons and on the other hand inhibited through the CVLM.