Regulation of sympathetic tone and arterial pressure by rostral ventrolateral medulla after depletion of Cl cells in rat

1. In this study we examined whether the rostral ventrolateral medulla (RVL M) maintains resting sympathetic vasomotor tone and activates sympathetic n erve activity (SNA) after the depletion of bulbospinal C1 adrenergic neuron es. 2. Bulbospinal C1 cells were destroyed (similar to 84% loss) by bilateral m icroinjections (spinal segments T-2-T-3) of an anti-dopamine-beta -hydroxyl ase antibody conjugated to the ribosomal toxin saporin (anti -D betaH-SAP). 3. Extracellular recording and juxtacellular labelling of bulbospinal baros ensitive neurones in the RVLM revealed that treatment with anti-D betaH-SAP spared the lightly myelinated neurones with no tyrosine hydroxylase immuno reactivity. 4. In rats treated with anti-D betaH-SAP, inhibition of RVLM neurones by bi lateral microinjection of muscimol eliminated splanchnic SNA and produced t he same degree of hypotension as in control rats. 5. Following treatment with anti-D betaH-SAP the sympathoexcitatory (splanc hnic nerve) and presser responses to electrical stimulation of the RVLM wer e reduced. 6. Treatment with anti-D betaH-SAP also eliminated the majority of A5 norad renergic neurones. However, rats with selective lesion of A5 cells by micro injection of beta -hydroxydopamine into the pens showed no deficits to stim ulation of the RVLM. 7. In summary, the loss of 84% of bulbospinal adrenergic neurones does not alter the ability of RVLM to maintain SNA and arterial pressure at rest in anaesthetized rats, but this loss reduces the sympathoexcitatory and presse r responses evoked by RVLM stimulation. The data suggest sympathoexcitatory roles for both the C1 cells and non-C1 cells of the RVLM and further sugge st the C1 cells are critical for the full expression of sympathoexcitatory responses generated by the RVLM.