Central nervous system modulation of baroceptor reflexes

Hockman, C.H.; Talesnik, J; Ke, Livingston

doi:10.1152/ajplegacy.1969.217.6.1681

Cited by 48 publications

(10 citation statements)

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“…The results of the present study also show that the baroreceptor reflex is modified during the initial five or ten seconds immediately after hypothalmic stimulation, but now it is the effect on blood pressure which is HYPOTHALAMUS AND BARORECEPTOR REFLEXES 481 reduced or absent whereas the normal bradyeardia may be very considerably enhanced. A similar pattern of alteration in heart rate responses to a rise in sinus pressure has been reported by Hockman, Talesnik & Livingston (1969) who found that the bradycardia induced by electrical stimulation of the sinus nerve was inhibited by simultaneous stimulation of the central grey matter of the mid-brain, but that immediately following such stimulation the bradyeardia was enhanced, and this facilitatory influence persisted for up to 10 see after the end of the stimulus. Hilton (1965) also noted that a marked bradycardia often occurred within a few seconds of stopping hypothalamic stimulation and attributed this to postinhibitory rebound of the baroreceptor reflex.…”

Section: Discussionsupporting

confidence: 80%

Modification of the reflex response to stimulation of carotid sinus baroreceptors during and following stimulation of the hypothalamic defence area in the cat

Humphreys¹,

Joels²,

McAllen³

1971

The Journal of Physiology

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3. During hypothalamic stimulation the reflex fall in blood pressure resulting from a rise in sinus pressure was found to be undiminished whether sinus pressure was raised at the onset or at the 10th sec of hypothalamic stimulation.4. By contrast, in at least half the cats in which a reflex bradyeardia could be evoked from the sinus, this bradycardia was largely if not completely suppressed during hypothalamic stimulation. This suppression of reflex bradycardia occurred when sinus pressure was raised at the onset as well as at the 10th sec of stimulation.5. During the first 5 sec after hypothalamic stimulation the hypotensive response to an increase in carotid sinus pressure was much reduced; on the other hand the reduction in heart rate was exaggerated, sometimes to a very marked degree.6. The results suggest that stimulation of the hypothalamic defence area can modify baroreceptor reflexes and that this modification can include selective alterations in the various components of the reflex response.

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Section: Discussionsupporting

confidence: 80%

Modification of the reflex response to stimulation of carotid sinus baroreceptors during and following stimulation of the hypothalamic defence area in the cat

Humphreys¹,

Joels²,

McAllen³

1971

The Journal of Physiology

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“…Similar inhibition of baroreflex was observed after the activation of other specific structures of the CNS, such as the hypothalamus (Bauer et al ., 1988) and the dorsolateral periaqueductal grey matter (Nosaka, 1996), areas that are known to receive projections from the vMPFC (Brown & Guyenet, 1985; Carrive et al ., 1988; Sesack et al ., 1989; Barman, 1990; Takagishi & Chiba, 1991; Fisk & Wyss, 2000; Vertes, 2004). The inhibition of baroreflex associated with these two areas is characterized by reduction of bradycardic responses, especially of vagal origin (Hockman et al ., 1969; Djojosugito et al ., 1970; Hockman & Talesnik, 1971; Coote et al ., 1979; Nosaka et al ., 1993). The similarity among responses suggests that these areas could be part of the neural pathway involved in the vMPFC‐related baroreflex modulation.…”

Section: Discussionmentioning

confidence: 99%

Medial prefrontal cortex NMDA receptors and nitric oxide modulate the parasympathetic component of the baroreflex

Resstel

Corrêa

2006

Eur J of Neuroscience

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The ventral portion of the medial prefrontal cortex (vMPFC) is involved in the modulation of the parasympathetic component of the baroreflex. In the present study, we verified the effect of blockade of vMPFC glutamatergic receptors and nitric oxide synthases (NOS) on the parasympathetic component of baroreflex in awake rats. Bilateral microinjection of the non-selective ionotropic glutamate antagonist kynurenic acid (KYN) into the vMPFC caused a shift of the threshold of reflex bradycardia toward higher pressures in response to increases in mean arterial pressure (MAP) caused by intravenous infusion of phenylephrine, thus indicating a tonic facilitatory influence action of vMPFC glutamate receptors on the parasympathetic component of the baroreflex. The effect of blockade of vMPFC-NMDA receptors by AP7 was similar to that observed after KYN, suggesting mediation via NMDA receptors. Pretreatment with the NOS inhibitor L-NAME or the specific neural NOS (nNOS) N(omega)-propyl-l-arginine microinjected in the vMPFC caused a shift of the reflex threshold toward higher pressures that was similar to that observed after blockade of NMDA receptors, thus indicating participation of the NO/NMDA-receptor pathway in the vMPFC modulation of the parasympathetic component of the baroreflex. In conclusion, our data indicate that glutamatergic neurotransmission in the vMPFC has a tonic facilitatory influence on the parasympathetic component of the baroreflex. Because local treatment with either the nNOS inhibitor N(omega)-propyl-l-arginine or the specific NMDA antagonist AP7 had similar effects on the baroreflex, it is also suggested that this modulation involves an NMDA-NO interaction within the vMPFC.

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“…It is now agreed that autonomic reflexes are influenced importantly by supramedullary components of the central nervous system (38)(39)(40)(41) and it should therefore not be surprising that general anesthesia modifies autonomic reflex control of the circulation (33,34). When electrical stimuli to the carotid sinus nerves of identical length, strength, and duration are applied to the same animals in the conscious and anesthetized states, different responses are evoked for heart rate, arterial pressure, and resistance in the peripheral beds.…”

Section: Effects Of Anesthesia On Circulatory Control Neural Control mentioning

confidence: 99%

Effects of Anesthesia on Cardiovascular Control Mechanisms

Vatner¹

1978

Environmental Health Perspectives

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Central nervous system modulation of baroceptor reflexes

Cited by 48 publications

References 0 publications

Modification of the reflex response to stimulation of carotid sinus baroreceptors during and following stimulation of the hypothalamic defence area in the cat

Modification of the reflex response to stimulation of carotid sinus baroreceptors during and following stimulation of the hypothalamic defence area in the cat

Medial prefrontal cortex NMDA receptors and nitric oxide modulate the parasympathetic component of the baroreflex

Effects of Anesthesia on Cardiovascular Control Mechanisms

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