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

Summary

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.

While the increase in activity of the splanchnic and renal sympathetic nerves and the rise in blood pressure due to hypothalamic stimulation were reduced by simultaneous bilateral sinus nerve stimulation or by an injection of clonidine, the evoked contractions of the nictitating membranes remained uninfluenced by both procedures. Thus, the effect of clonidine resembles an activation of the depressor baroreceptor reflex in inhibiting preferentially the activity in adrenergic vasomotor fibres. This and the clonidine-induced facilitation of the reflex suggest an intimate relationship between the action of clonidine and an activation of the central pathway of the depressor baroreceptor reflex.