Bradycardia evoked by hypothalamic stimulation in the rabbit: Dependence upon the arterial blood pressure

Effects of some α‐adrenoceptor antagonists on central cardio‐decelerator mechanisms in the rabbit

“…administration of these drugs has always been complicated by their peripheral vasodepressor action. The intensity of the cardio-decelerator response is approximately proportional to the value of the mean arterial blood pressure above a threshold value (Buss & Evans, 1984) and, in addition, pressor responses that usually accompany the cardio-deceleration presumably add to the overall bradycardia. Evans et al (1983) lowered blood pressure by haemorrhage to obtain control values of -AHR: BP, with which to compare the drug effects, but haemorrhage was an imperfect control because it allowed the pressor responses to remain more-or-less unchanged, compared to the reduced responses recorded after many a-adrenoceptor antagonists.…”

“…It is known that electrical stimulation in the brainstem of the anaesthetized rabbit can cause cardio-deceleration (Evans, 1976;Sampson et al, 1977;Gellman et al, 1981). Stimulation in the zona incerta and lateral hypothalamic area close to the mammillothalamic tract evokes bradycardia by a mechanism in which a projection from the stimulated area appears to raise the gain of the cardio-inhibitory limb of the baroreceptor reflex (Evans, 1978;Buss & Evans, 1984). There have been indications that this increase in gain could be blocked by some a-adrenoceptor antagonists which did not block the baroreceptor reflex itself (Powell et al, 1972;Evans, 1980;Evans et al, 1983).…”

“…Because stimulation simultaneously evoked arterial pressor responses, which were also attenuated by the phentolamine, these authors concluded that the bradycardia was mainly a baroreflex response to the rise in arterial blood pressure. Evans (1978) showed that the cardio-deceleration evoked by stimulation of the posterior hypothalamus in the anaesthetized rabbit was sometimes too great to be accounted for by a baroreceptor reflex activated during the accompanying rise in arterial blood pressure, and there is evidence that a pathway from this part of the rabbit hypothalamus acts on the baroreceptor reflex so as to increase the gain of the cardio-inhibitory mechanism (Buss & Evans, 1984). Manchanda et al (1977) have found that phenoxybenzamine abolished some cardiovascular responses associated with stimulation of the hypothalamic 'defence area' in dog and cat, following either intravenous administration or topical injection into the hypothalamus.…”