CNS SITE OF BETA-ADRENERGIC BLOCKER-INDUCED HYPOTENSION IN THE CAT - MICROIONTOPHORETIC STUDY OF BULBAR CARDIOVASCULAR NEURONS

For the purpose of localizing the central site and mechanism of β-adrenergic blocker-induced hypotension, propranolol and sotalol were applied by the technique of microiontophoresis to neurones of the bulbar cardiovascular centre in midcollicular decerebratc cats. The excitatory and inhibitory cardiovascular neurones were identified by their response to an increase in the arterial blood pressure induced by intravenous injections of small doses of norepinephrine (NE). Both β-adrenergic blockers exhibited an inhibitory effect on the spontaneous firing rate of excitatory cardiovascular neurones but had no effect on the firing rate of inhibitory cardiovascular neurones. At the same or greater doses, they had no effect on the firing rate of noncardiovascular neurones recorded from the same area. However, at high doses, only propranolol produced a reduction of spike amplitude on each of the 3 types of neurones, indicative of a nonspecific local anaesthetic action which was unrelated to propranolol-induced cardiovascular neurone slowing. In 3 control experiments, sodium nitrite, a direct acting vasodilator agent, was found to have no effect on the activity of the cardiovascular neurones. While these results cannot exclude the possibility of a peripheral influence in β-adrenergic blocker induced-hypotension, it is concluded that the major hypotensive effect is the result of their action on β-adrenergic receptors of bulbar cardiovascular neurones. © 1979.