Buffer reflexes, tolerance to ganglioplegics and their relationship to enhanced pressor responsiveness

Tetraethylammonium, hexamethonium, chlorisondamine or mecamylamine suppressed the dog's carotid occlusion reflex well before appearance of maximum augmentation of responses to pressor drugs. The reflex usually returned to near control values despite continued administration of ganglioplegics, while augmented responsiveness persisted or became more marked. An antipseudocholinesterase or prostigmine restored the suppressed reflex without loss of augmented responsiveness. Electroneurographic measurements of efferent spontaneous activity in postganglionic renal nerves revealed synaptic pathways resistant to blockade: a small amount of activity persisted during tolerance to ganglioplegics and showed reflex changes. Similar measurements of spontaneous and evoked potentials in the inferior cardiac nerve showed no synaptic activity during tolerance. Augmentation of response to pressor drugs by ganglioplegics does not depend wholly upon loss of compensatory reflexes; peripheral sensitization is probably another mechanism concerned. Maintenance of arterial pressure and persistence of cardiovascular reflexes during tolerance to ganglioplegics appear to depend upon transmission of a relatively few impulses over pathways resistant to blockade and upon peripheral sensitization to the presumably smaller amounts of norepinephrine released from nerve endings.