Research ReportCentral cholinergic blockade reduces the pressor response to l-glutamate into the rostral ventrolateral medullary pressor area

Injections of the excitatory amino acid l-glutamate (l-glu) into the rostral ventrolateral medulla (RVLM) directly activate the sympathetic nervous system and increase mean arterial pressure (MAP). A previous study showed that lesions of the anteroventral third ventricle region in the forebrain reduced the pressor response to l-glu into the RVLM. In the present study we investigated the effects produced by injections of atropine (cholinergic antagonist) into the lateral ventricle (LV) on the pressor responses produced by l-glu into the RVLM. Male Holtzman rats (280-320 g, n = 5 to 12/group) with stainless steel cannulas implanted into the RVLM, LV or 4th ventricle (4th V) were used. MAP and heart rate (HR) were recorded in unanesthetized rats. After saline into the LV, injections of l-glu (5 nmol/100 nl) into the RVLM increased MAP (51 ± 4 mm Hg) without changes in HR. Atropine (4 nmol/1 μl) injected into the LV reduced the pressor responses to l-glu into the RVLM (36 ± 5 mm Hg). However, atropine at the same dose into the 4th V or directly into the RVLM did not modify the pressor responses to l-glu into the RVLM (45 ± 2 and 49 ± 4 mm Hg, respectively, vs. control: 50 ± 4 mm Hg). Central cholinergic blockade did not affect baro and chemoreflex nor the basal MAP and HR. The results suggest that cholinergic mechanisms probably from forebrain facilitate or modulate the pressor responses to l-glu into the RVLM. The mechanism is activated by acetylcholine in the forebrain, however, the neurotransmitter released in the RVLM to facilitate the effects of glutamate is not acetylcholine.