Circulatory Effects of Interruption and Stimulation of Cardiac Vagal Afferents

ÖBerg, Bengt; White, Saxon William

doi:10.1111/j.1748-1716.1970.tb04802.x

Cited by 108 publications

(44 citation statements)

References 15 publications

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“…19 There are, in addition, data to suggest that vagally innervated cardiopulmonary receptors are preferentially oriented toward renal vasomotor neurons. 22 ' 23 The findings of this study are in agreement with these earlier observations. Vagal cold block at a carotid sinus pressure of 40 mm Hg caused a mean increase of 30 mm Hg in systemic arterial pressure and a mean decrease of 42 ml/min in renal blood flow.…”

Section: Discussionsupporting

confidence: 93%

Release of renin by the carotid baroreflex in anesthetized dogs. Role of cardiopulmonary vagal afferents and renal arterial pressure.

Jarecki¹,

Thorén²,

Donald³

1978

Circ Res

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SUMMARY In 3 of 10 anesthetized dogs with aortic nerves sectioned and renal arterial pressure maintained constant, reduction to 40 mm Hg of the pressure in the vascularly isolated carotid sinuses resulted in an increase in renin secretion. After section of the vagus nerves, carotid sinus hypotension resulted in an increase in renin secretion in 9 of the 10 dogs. Vagal nerve section in these 10 dogs with carotid sinuses vascularly isolated and maintained at a pressure equal to existing aortic pressure resulted in significant increases in basal levels of plasma renin activity and renin secretion. The increase in renin secretion found during carotid sinus hypotension in vagotomized dogs was totally or substantially inhibited when renal arterial pressure was not maintained constant but allowed to increase equally with systemic arterial pressure. The increase in renin secretion observed during carotid hypotension in vagotomized dogs with renal arterial pressure held constant was abolished by renal denervation. We conclude that the carotid baroreflex is involved in the neural control of renin release. However, a concomitant activation of cardiopulmonary receptors and/or a substantial rise in renal arterial pressure can suppress the reflex increase in the secretion of renin induced by carotid sinus hypotension. have shown that the release of renin in such diverse situations as suprarenal aortic stenosis, administration of the diuretic furosemide, and tilting to the upright position is dependent on neural mechanisms in considerable degree. In view of these observations, it is surprising to find disagreement regarding the role of the carotid baroreflex in the control of renin secretion. Three studies"*" 12 reported an increase in renin secretion during carotid occlusion and three studies 13 " 15 reported that renin secretion was not affected by changes in carotid sinus pressure. IN THE LAST FEW YEARS increasing attention hasIn a recent study it was shown that, when the carotid sinus was free to exert its buffering influence, complete interruption of afferent vagal nerve traffic from cardiopulmonary receptors did not result in an increase in renin secretion in 17 of 20 dogs. 16 Because it has been shown that the inhibitory influence of vagally innervated cardio- pulmonary receptors becomes more pronounced as that of the carotid baroreceptors is reduced," it seemed possible that this interaction between the two receptor systems might act to inhibit the release of renin during carotid sinus hypotension. The following studies were carried out to investigate this question. MethodsDogs weighing 16-20 kg were maintained on a daily intake of 65 mEq of Na + and 55 mEq of K + for 5 days before study. Anesthesia was induced with sodium thiopental (30 mg/kg, intravenously) followed by a-chloralose (80 mg/kg dissolved in 5% dextrose in water and administered intravenously). Supplemental doses of chloralose (5-10 mg/kg) were given hourly. Gallamine triethiodide (Flaxedil; 3 mg/kg, iv) was used to obtain muscle relaxation during the su...

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Section: Discussionsupporting

confidence: 93%

Release of renin by the carotid baroreflex in anesthetized dogs. Role of cardiopulmonary vagal afferents and renal arterial pressure.

Jarecki¹,

Thorén²,

Donald³

1978

Circ Res

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“…The existence of non-myelinated vagal efferent axons in cardiac and pulmonary branches has also been demonstrated histologically (Agestoni et al 1957 (Amman & Schaefer, 1943;Jarisch & Zottermann, 1948;Dickinson, 1950;Neil & Zottermann, 1950;Oberg & Thoren, 1972;Thoren, 1976Thoren, , 1977, and these branches also contain afferent fibres from the lungs (Dickinson, 1950 ;Oberg&Thoren, 1973;Donoghue, Fox&Kidd, unpublished observations (Lipski, McAllen & Spyer, 1975;Jordan & Spyer, 1977;Berger, 1979;Panneton & Loewy, 1980 Neurones activated by non-myelinated cardiac afferent fibres were not found in the nucleus ambiguus. This is surprising since such afferent fibres are known to produce a profound vagal bradycardia when excited (Oberg & White, 1970;Oberg & Thoren, 1973), and it is known that cardiomotor efferent neurones lie in this area (McAllen & Spyer, 1976. However, the cells are sparse and in our study a specific search was not made for neurones with myelinated axons excited antidromically from the cardiac branch.…”

Section: Discussionmentioning

confidence: 66%

The Distribution in the Cat Brain Stem of Neurones Activated by Vagal Non‐myelinated Fibres From the Heart and Lungs

et al. 1981

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SUMMARYIn anaesthetized cats, right cardiac vagal branches were electrically stimulated and recordings of evoked 'slow wave' and single neurone activity were made in the brain stem. Short-latency ' slow wave' and multi-neuronal activity evoked by excitation ofmyelinated vagal afferent fibres were recorded in the medial and lateral subnuclei of the nucleus tractus solitarius, the area postrema, the dorsal vagal motor nucleus, the lateral reticular formation and the nucleus ambiguus. Long-latency responses evoked by vagal non-myelinated fibres were recorded in the medial subnucleus of the nucleus tractus solitarius, the area postrema, dorsal vagal motor nucleus, the parahypoglossal area and the lateral reticular formation dorsal to the nucleus ambiguus. A specific study was made ofseventy-two single neurones activated by non-myelinated afferent fibres in the cardiac branch. Thirty-four were shown to be synaptically activated, twenty-one were activated nonsynaptically and seventeen could not be classified. One neurone was also activated by myelinated cardiac afferent fibres, and two by thoracic vagal (including pulmonary) afferent fibres. Neurones were not spontaneously active. Indirect evidence suggests that the majority of the recordings of nonsynaptically activated neurones were likely to be from cell bodies. Neurones were located from the level of the obex to 3*0 mm rostral to it in the medial subnucleus of the nucleus tractus solitarius (45), and in the lateral subnucleus (2), the area postrema and its border with the medial subnucleus of the nucleus tractus solitarius (13), the dorsal vagal motor nucleus (9), the parahypoglossal area (1) and the lateral reticular formation dorsal to nucleus ambiguus (2). Recordings were made from fifteen neurones activated by myelinated fibres in the cardiac vagal branches, and twelve were excited synaptically. The neurones were located in the medial (8) and lateral (3) subnuclei of the nucleus tractus solitarius, the dorsal vagal motor nucleus (1) and the lateral reticular formation (1). Four neurones were also excited by vagal afferent fibres in the thoracic vagal nerve immediately caudal to the caudal cardiac branch.

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“…A final possibility is that the tonic influence of CPBR might not be easily detected from changes in heart rate, hindlimb perfusion pressure, or arterial pressure, but might be more evident if one examined changes in sympathetic outflow to other beds, such as the kidney (Thoren, 1979). All three of these points may be valid and have been suggested in other published work (Oberg and White, 1970;Mancia et al, 1973;Thoren, 1979).…”

Section: Tonic Influences Of Vagal Afferentsmentioning

confidence: 94%

Differential baroreflex control of heart rate and vascular resistance in rabbits. Relative role of carotid, aortic, and cardiopulmonary baroreceptors.

Guo¹,

Thames²,

Abboud³

1982

Circ Res

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SUMMARY. We assessed the relative roles of aortic (ABR), carotid sinus (CBR), and vagal cardiopulmonary baroreceptors in the reflex control of heart rate and vascular resistance during changes in arterial blood pressure. Injections of phenylephrine (PE) and nitroglycerin (NG) were given intravenously to anesthetized rabbits (chloralose-urethane). Reflex heart rate responses were impaired significantly by denervation (X) of either CBR or ABR. In contrast, reflex vascular responses in the hindlimb (perfused at constant blood flow) were preserved except for a slight impairment of reflex vasoconstriction after ABRX. Vagotomy with intact CBR and ABR impaired only the reflex bradycardia. After vagotomy, neither CBRX nor ABRX altered significantly the reflex heart rate or vascular responses except, again, for an impairment of reflex vasoconstriction after ABRX. Combined CBRX and ABRX eliminated all reflex responses except for a small bradycardia and a biphasic change in perfusion pressure (constrictor-dilator) during PE. Vagotomy eliminated the bradycardia and the dilator phase; the constrictor phase persisted and was abolished by lumbar sympathectomy. The results indicate that (1) reflex control of heart rate may be impaired when reflex control of hindlimb resistance is preserved; thus reflex changes in heart rate may not be used as a reliable index of the integrity of arterial baroreceptor control of the total circulation; (2) one set of arterial baroreceptors does not compensate for the absence of the other with respect to activation of vagal neurons; in contrast, one set of baroreceptors compensates fully for the absence of the other with respect to inhibition of sympathetic neurons; (3) cardiopulmonary and other baroreceptors contribute minimally to reflex responses only during large PE-induced increases in arterial pressure. (Circ Res 50: 554-565, 1982)

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Circulatory Effects of Interruption and Stimulation of Cardiac Vagal Afferents

Cited by 108 publications

References 15 publications

Release of renin by the carotid baroreflex in anesthetized dogs. Role of cardiopulmonary vagal afferents and renal arterial pressure.

Release of renin by the carotid baroreflex in anesthetized dogs. Role of cardiopulmonary vagal afferents and renal arterial pressure.

The Distribution in the Cat Brain Stem of Neurones Activated by Vagal Non‐myelinated Fibres From the Heart and Lungs

Differential baroreflex control of heart rate and vascular resistance in rabbits. Relative role of carotid, aortic, and cardiopulmonary baroreceptors.

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