Mechanism of Hypothalamic Control of Cardiac Component of Sinus Nerve Reflex

Lopes, Oswaldo Ubrı́aco; Palmer, Jeffrey M.

doi:10.1113/expphysiol.1978.sp002438

Cited by 20 publications

(14 citation statements)

References 21 publications

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“…Our observations on the interactions between laryngeal activation and the defence response are not in agreement with those of Lopes & Palmer (1978). These authors substantiated the earlier observations that HDA stimulation could suppress the bradycardia that normally accompanies baroreceptor stimulation (see Hilton, 1966).…”

Section: Discussionsupporting

confidence: 73%

Hypothalamic modulation of laryngeal reflexes in the anaesthetized cat: role of the nucleus tractus solitarii.

Dawid-Milner¹,

Silva-Carvalho²,

Goldsmith³

et al. 1995

The Journal of Physiology

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1. This investigation was initiated because activation of laryngeal afferents, either by electrical stimulation of the superior laryngeal nerve (SLN) or by natural stimulation of receptors in the laryngeal mucosa, results in a cardiorespiratory response comprising bradycardia, hypotension and apnoea (phrenic nerve activity was suppressed). This pattern of response is qualitatively equivalent to the response that is evoked on activation of the arterial baroreceptors. 2. Preliminary studies indicated that the effects of activating the SLN were suppressed during stimulation in the hypothalamic defence area (HDA) at points that also blocked the effects of baroreceptor stimulation. 3. Recordings were taken from seventy-two neurones localized within the ipsilateral nucleus tractus solitarii (NTS) whose activity was modified by SLN stimulation. Sixty neurones responded with an EPSP on SLN stimulation; nine of these had an inspiratory firing pattern. Five neurones were seen to receive an IPSP on SLN stimulation. 4. Five respiratory SLN-activated neurones were unresponsive to stimulation of the other nerve inputs, whilst four received convergent EPSP inputs on sinus nerve (SN) stimulation. One cell of these four also received inputs from the aortic and the vagus nerves. Sixty-one non-respiratory SLN-activated neurones also received convergent inputs from the sinus nerve. Of these, fifty displayed an EPSP, four an IPSP and seven an EPSP-IPSP. Fifteen neurones also received inputs from the aortic nerve and seventeen from the vagus. 5. From the population of neurones affected by SLN stimulation, twenty-four of seventy were also influenced by HDA stimulation (3 were respiratory cells). Sixteen of these responses consisted of an EPSP (2 respiratory cells), five of an IPSP (1 respiratory cell) and three of an EPSP-IPSP. 6. In neurones receiving an IPSP on HDA stimulation, the SLN-evoked excitatory response was reduced throughout the period of HDA-evoked inhibition. These neurones were all shown to receive excitatory inputs from the arterial baroreceptors and laryngeal mechanoreceptors. 7. Additionally, in the thirty-seven neurones that were excited by SLN stimulation but received no direct synaptic input on HDA stimulation, a conditioning stimulus to the HDA evoked a block of SLN-evoked responses without an accompanying change in membrane potential. Several of these neurones were also affected by both baroreceptor and laryngeal mechanoreceptor stimulation. 8. These observations are discussed in the context of the role of the NTS in cardiorespiratory control. The potential importance of these interactions in respiratory distress are highlighted and the implications for the organization of central pathways for the control of autonomic and respiratory function are discussed.

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Section: Discussionsupporting

confidence: 73%

Hypothalamic modulation of laryngeal reflexes in the anaesthetized cat: role of the nucleus tractus solitarii.

Dawid-Milner¹,

Silva-Carvalho²,

Goldsmith³

et al. 1995

The Journal of Physiology

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“…There is an accompanying pressor response, but the cardioinhibition which one would expect to result from activation of the baroreceptor reflexes is itself inhibited during the period of stimulation [Achari, Al-Ubaidy and Downman, 1973;Coote et al, 1979;Djojosugito et al, 1970;Hilton, 1963]. This inhibition of baroreflex bradycardia may be mediated through an inspiratory 'gating' mechanism, tonically activated during 'defence area' stimulation [Lopes and Palmer, 1978]. Active muscle vasodilatation is one of the most characteristic features of the carnivore 'defence reaction' [Abrahams et al, 1960;Eliasson et al, 1951;Hilton, 1966] and the additional cardiac output goes mainly to supply the skeletal muscles [Folkow et al, 1968].…”

Section: Discussionmentioning

confidence: 99%

“…Stimulation of the 'defence area' in the anaesthetized cat evokes tachycardia [Eliasson, Folkow, Lindgren and Uvnas, 1951] during which the baroreflex cardioinhibition that would have accompanied the rise in blood pressure is inhibited by influences from the hypothalamus [Coote, Hilton and Perez-Gonzalez, 1979;Djojosugito, Folkow, Kylstra, Lisander and Tuttle, 1970;Hilton, 1963;Lopes and Palmer, 1978]. In M.8 M. II.…”

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confidence: 99%

An Effect of Hypothalamic Stimulation on Cardiac Output in the Rabbit

Evans

1980

Exp Physiol

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Electrical stimulation of a discrete region of the rabbit brainstem, in the lateral hypothalamic area near the mammillothalamic tract, caused an increase in arterial blood pressure accompanied by bradycardia in anaesthetized animals. Stimulation of the brainstem of the anaesthetized rabbit, in a small region of the lateral hypothalamic area dorsal to the lateral mammillary nucleus and near to the mammillothalamic tract 1-2mm from the midline, can evoke peripheral vasoconstriction with rises in arterial blood pressure and bradycardia. During strong stimulation the heart rate may fall to 20-30 % of the resting rate. These cardiovascular responses may be accompanied by signs of arousal, pupillodilatation, exophthalmos and a transient apnoea or shallow tachypnoea superimposed on a tonic inspiratory effort [Evans, 1976[Evans, , 1980Evans and Pepler, 1974].Although the location of this responsive point in the rabbit hypothalamus bears some resemblence to the caudal extension of the so-called 'defence area' of the cat [Abrahams, Hilton and Zbrozyna, 1960; Hess and Briigger, 1943] and although several of the effects mentioned above have also been obtained by stimulation of the 'defence area' in the cat, the chronotropic responses of the heart are qualitatively opposite in these two species. Stimulation of the 'defence area' in the anaesthetized cat evokes tachycardia [Eliasson, Folkow, Lindgren and Uvnas, 1951] during which the baroreflex cardioinhibition that would have accompanied the rise in blood pressure is inhibited by influences from the hypothalamus

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confidence: 99%

“…Their role is made even more significant by the fact that many of the NTS neurones that are known to receive an input from the arterial baroreceptors, and an inhibitory control from the hypothalamus, also respond to activation of vagal afferents, including those that relay in the superior laryngeal nerve (Biscoe & Sampson, 1970;Mufflin et al 1988a, b). Hence, the activation of the HDA has the potential to modulate other reflexes (Lopes & Palmer, 1978) and this is considered in fuller detail in accompanying papers (Dawid-Milner, SilvaCarvalho, Goldsmith & Spyer, 1995; Silva-Carvalho, Dawid-Milner, Goldsmith & Spyer, 1995 (VN) and superior laryngeal nerve (SLN) were isolated for electrical stimulation (1-2 pulses, 0-1ms, 1-20 V given at 1 Hz). A SwanGanz catheter was advanced via the external carotid artery into the right carotid sinus.…”

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confidence: 99%