Further similarities between the action of clonidine and a central activation of the depressor baroreceptor reflex.

Abstract

The relationship between the central action of the hypotensive drug clonidine and the depressor baroreceptor reflex was studied in cats anaesthetized with urethane. Activation of the depressor baroreceptor reflex was achieved by bilateral electrical stimulation of the sinus nerves. The magnitude of the activation of the reflex was estimated from the resultant decrease in spontaneous sympathetic activity recorded from the preganglionic splanchnic and a postganglionic renal nerve and from the subsequent fall in blood pressure. The effect of bilateral sinus nerve stimulation was frequency-dependent over the range of 2 to 32 shocks/sec and allowed the construction of frequency-response curves. Clonidine in low doses (1 and 3 μg/kg i.v.), which caused no or only a slight depression of spontaneous sympathetic nerve activity and of the blood pressure, increased the response to bilateral sinus nerve stimulation with a resultant shift of the respective frequency-response curves to lower rates of stimulation. Clonidine also augmented the bradycardia produced by an activation of the depressor baroreceptor reflex. These results indicate a facilitation of the depressor baroreceptor reflex by clonidine.