Do adrenaline-containing neurones from the rostral ventrolateral medulla excite preganglionic sympathetic cell...

Experiments were performed to investigate whether descending vasomotor neurones from the rostral ventrolateral medulla (RVL) utilize adrenaline as a neurotransmitter. Electrical stimulation of the RVL caused marked, short lasting, reproducible increases in blood pressure and heart rate in anaesthetised atropine methylbromide-treated rats. These effects probably reflect activation of cell bodies rather than fibres of passage since injection of L-glutamate into the same area also produced tachycardia and vasopressor responses. The effects of RVL stimulation were unchanged after bilateral adrenalectomy but were markedly reduced by guanethidine (1 mg/kg, i.v.) suggesting that the tachycardia and vasopressor responses were mediated via increased sympathetic tone to the heart and vasculature. Pretreatment with the phenylethanolamine-N-methyl transferase (PNMT) inhibitor LY134046 (1 mg intracisternally, and 40 mg/kg i.p. daily for 1 day or 5 days) did not modify either the tachycardia or vasopressor response to stimulation of the RVL. Resting blood pressure and heart rate were also unchanged. Cardiac preganglionic sympathetic nerves supplying the heart arise from the C7-T2 region of the spinal cord. Phentolamine and propranolol were injected intrathecally (i.t.) in this region, in an attempt to block the spinal receptors at which any adrenaline, released locally during RVL stimulation, might be expected to act in order to elicit the characteristic tachycardia. Phentolamine (10 and 100 micrograms i.t.) and propranolol (1 microgram i.t.) did not modify the tachycardia but propranolol (10 and 100 micrograms i.t.) caused a dose-dependent reduction. These doses of propranolol (10 and 100 micrograms i.t.) also produced blockade of peripheral beta-adrenoreceptors. The failure of PNMT inhibition to modify the tachycardia or vasopressor response to RVL stimulation and the lack of effect of intrathecally injected alpha-and beta-adrenoreceptor antagonists (at doses which do not exert peripheral effects) against the RVL stimulation-induced tachycardia suggests that adrenaline does not subserve a spinal neurotransmitter role, at the C7-T2 region.