In anaesthetized and bilaterally vagotomized dogs, reflex
bradycardia elicited by
intravenous injection of
noradrenaline was facilitated by
AR-C 239, a new alpha 1-adrenoceptor blocking
drug and inhibited by the alpha 2-adrenoceptor antagonist,
yohimbine. Both alpha-blocking drugs were administered into the vertebral artery. In another group of bilaterally vagotomized dogs, unilateral electrical stimulation of the carotid sinus nerve induced a frequency-dependent decrease in mean blood pressure solely mediated through the sympatho-inhibitory component of the baroreflex. Administration of the alpha 1-adrenoceptor blocking drugs,
AR-C 239 and
prazosin (5 micrograms/kg) into the vertebral artery decreased basal mean blood pressure and increased depressor responses to the carotid sinus nerve stimulation, whereas the intracisternal injection of
phenylephrine (30 micrograms/kg), a preferential alpha 1-agonist, increased mean blood pressure but inhibited the
hypotension resulting from electrical stimulation. In addition, the injection into the vertebral artery of
yohimbine (100 micrograms/kg), an alpha 2-adrenoceptor blocking agent which caused no change in mean arterial pressure, inhibited the decrease in the sympathetic component. In conclusion, these results suggest the possible participation of the two types of alpha-
adrenoceptors in the modulation of the sympathetic component of the baroreflex: alpha 1-adrenoceptor stimulation could inhibit, whereas alpha 2-adrenoceptor activation facilitates the reflex activity in the sympathetic fibres.