Central organization and interaction of the carotid baroreceptor and chemoreceptor sympathetic reflex

Trzebski, A; Lipski, Janusz; Majcherczyk, S; Szulczyk, Paweł; ́cielewski, L. Chrus

doi:10.1016/0006-8993(75)90420-5

Cited by 29 publications

(10 citation statements)

References 30 publications

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“…31 Another possibility may be some inhibition in the central chemoreceptor pathways as a result of antagonistic interaction between arterial baro-and chemoreceptor reflexes. 40 Increased carotid baroreflex gain during postexercise period has been observed. 12,14,15 Healthy subjects breathing high oxygen exhibit reduced heart rate and cardiac output parallel with augmented TPR.…”

Section: Discussionmentioning

confidence: 99%

Postexercise decrease in arterial blood pressure, total peripheral resistance and in circulatory responses to brief hyperoxia in subjects with mild essential hypertension

et al. 1998

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The objective of our study was: (1) to compare the influence of moderate exercise on circulatory afterresponse in mildly hypertensive (n = 8) and normotensive male subjects (n = 9); (2) to examine the circulatory response to 3-min hyperoxic inactivation of arterial chemoreceptors at rest and during postexercise period in both groups. Hypertensive men (HTS) with a systolic blood pressure (SBP) 148 ؎ 5 mm Hg, diastolic blood pressure (DBP) 92.4 ؎ 4 mm Hg; and normotensive men (NTS), with a SBP 126 ؎ 3 mm Hg, DBP 75.6 ؎ 1.3 mm Hg, were submitted to 20-min of moderate exercise on a cycloergometer (up to the level of 55% of each subject's resting heart rate reserve). Finger arterial BP was recorded continuously with Finapres, impedance reography was used for recording stroke volume, cardiac output and arm blood flow. In HTS a significant decrease in SBP by 14.5 ؎ 3.4 mm Hg, DBP by 8.9 ؎ 1.9

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Section: Discussionmentioning

confidence: 99%

Postexercise decrease in arterial blood pressure, total peripheral resistance and in circulatory responses to brief hyperoxia in subjects with mild essential hypertension

et al. 1998

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“…Recording in the nucleus of the tractus solitarius from cells excited by electrical stimuli applied to the carotid sinus nerve, Trzebski et al (1975) found the spread of latencies to be from 3 to 21 ms. Even allowing a conduction distance of 5 cm from carotid sinus to medulla in the dog, a spread of only -50 ms could be accounted for between afferents conducting at 1 m/s and 100 m/s, but the cardiac vagal response outlasts the stimulus which evokes it by 500 ms or more.…”

Section: Discussionmentioning

confidence: 99%

“…Trzebski, Lipski, Majcherczyk, Szulczyk & Chruscielewski (1975) recorded in the nucleus of the tractus solitarius from eightyfour cells which were excited by electrical stimuli applied to the carotid sinus nerve, and reported post-excitatory depression lasting 'up to several hundred milliseconds' in twenty-three of these. Whether or not these cells were relays to cardiac vagal motoneurones, however, was not determined.…”

Section: Discussionmentioning

confidence: 99%

Excitation and inhibition of cardiac vagal motoneurones by electrical stimulation of the carotid sinus nerve.

McCloskey¹,

Potter²

1981

The Journal of Physiology

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SUMMARY1. The carotid sinus nerve was electrically stimulated in dogs anaesthetized with chloralose. Stimuli (1 ms, 1-10 V, < 1 Hz) evoked responses in single cardiac efferent fibres dissected from the cervical part of the vagus nerve. The mean latencies of these responses varied, from fibre to fibre, between 30 and 120 ms.2. Stimuli given during the expiratory phase of the respiratory cycle evoked vagal responses with a shorter latency than similar stimuli given only during the inspiratory phase of the respiratory cycle.3. Following the vagal response to carotid sinus nerve stimulation a period of inhibition of vagal activity, lasting 100-150 ms, occurred. Refractoriness of the responding vagal motoneurone following an action potential could not account for this post-excitatory depression.4. The inhibitory effects of electrical stimulation of the carotid sinus nerve were further studied by applying pairs of similar electrical stimuli to the carotid sinus nerve. The second stimulus of a pair had to be given 80-100 ms after the first to evoke a second response.5. Trains of electrical stimuli (30-100 Hz) were also studied. At low frequencies the inhibitory effect of successive stimuli on vagal responses became less marked, but at higher frequencies only the first and last stimulus of the train reliably evoked responses. For trains of stimuli at both low and high frequencies, the last stimulus of the train evoked a vagal response, which was succeeded by a period of inhibition of vagal firing: this inhibition was then followed by further excitation before vagal discharge returned to resting levels.

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“…Considerable interaction is known to occur between baroreceptor and CB chemoreceptor control of sympathetic nerve activity (Trzebski et al 1975,Somers et al1991. The two afferent inputs have a mutual inhibitory interaction on sympathetic outflow: baroreceptor input suppresses chemoreflex activation of sympathetic outflow and chemoreceptor input suppresses baroreflex inhibition of sympathetic outflow (Wennergren et al 1976).…”

Section: Central Interaction With Other Reflexes and Brainstem Mechanmentioning

confidence: 99%

Carotid body function in heart failure

Schultz

2007

Respiratory Physiology & Neurobiology

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In this review, we summarize the present state of knowledge of the functional characteristics of the carotid body (CB) chemoreflex with respect to control of sympathetic nerve activity (SNA) in chronic heart failure (CHF). Evidence from both CHF patients and animal models of CHF has clearly established that the CB chemoreflex is enhanced in CHF and contributes to the tonic elevation in SNA. This adaptive change derives from altered function at the level of both the afferent and central nervous system (CNS) pathways of the reflex arc. At the level of the CB, an elevation in basal afferent discharge occurs under normoxic conditions in CHF rabbits, and the discharge responsiveness to hypoxia is enhanced. Outward voltage-gated K + currents (I K ) are suppressed in CB glomus cells from CHF rabbits, and their sensitivity to hypoxic inhibition is enhanced. These changes in I K derive partly from downregulation of nitric oxide synthase (NOS) / NO signaling and upregulation of angiotensin II (Ang II) / Ang II receptor (AT 1 R) signaling in glomus cells. At the level of the CNS, interactions of the enhanced input from CB chemoreceptors with altered input from baroreceptor and cardiac afferent pathways and from central Ang II further enhance sympathetic drive. In addition, impaired function of NO in the paraventricular nucleus of the hypothalamus participates in the increased SNA response to CB chemoreceptor activation. These results underscore the principle that multiple mechanisms involving Ang II and NO at the level of both the CB and CNS represent complementary and perhaps redundant adaptive mechanisms to enhance CB chemoreflex function in CHF.

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Central organization and interaction of the carotid baroreceptor and chemoreceptor sympathetic reflex

Cited by 29 publications

References 30 publications

Postexercise decrease in arterial blood pressure, total peripheral resistance and in circulatory responses to brief hyperoxia in subjects with mild essential hypertension

Postexercise decrease in arterial blood pressure, total peripheral resistance and in circulatory responses to brief hyperoxia in subjects with mild essential hypertension

Excitation and inhibition of cardiac vagal motoneurones by electrical stimulation of the carotid sinus nerve.

Carotid body function in heart failure

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