Endogenous GABAergic mechanisms in the medulla and the regulation of blood pressure

In the present study, the γ-aminobutyric acid receptor antagonist, bicuculline methiodide (BMI), was used to explore the role of endogenous medullary GABAergic mechanisms in the neural control of circulation. In urethane-anesthetized rats, microinjections of the neuroexcitatory amino acid, L-glutamate (150-300 ng/site) were used to functionally identify rostral ventrolateral vasopressor neuron pools (VLPA) and caudal ventrolateral vasodepressor neuron pools (VLDA). The bilateral microinjection of BMI into the ventrolateral vasodepressor neuron pool caused a dose-related (0.1-100.0 ng/site) decrease in blood pressure (BP), pulse pressure and heart rate (HR). Maximum decreases in BP and HR were 51 ± 2 mm Hg and 245 ± 9 beats/min, respectively. In the VLPA, BMI caused a dose-related (0.1-100.0 ng/site) increase in BP, HR and pulse pressure. Maximum increases in BP and HR were 88 ± 3 mm Hg and 73 ± 4 beats/min, respectively. In the VLPA, BMI also caused a 40% increase in the carotid artery occlusion response and a 48% reduction in the aortic depressor nerve response. It seems plausible that GABAergic mechanisms in both the caudal and rostral ventrolateral medulla are tonically involved with the maintenance and reflex regulation of vasomotor activity. Medullary γ-aminobutyric acid may provide a reciprocal inhibitor between rostral vasopressor and caudal vasodepressor neuron pools.