Circulatory Responses to Stimulation of Medullated and Non‐medullated Afferents in the Cardiac Nerve in the Cat

ÖBerg, Bengt; Thorén, Peter

doi:10.1111/j.1748-1716.1973.tb05373.x

Cited by 89 publications

(19 citation statements)

References 25 publications

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“…To simplify the study procedures, we evaluated the reflex vascular response to LBNP by measuring the changes in TPR induced by LBNP. This approach might appear to conflict with the data of Oberg and Thoren, 24 who reported that cardiopulmonary receptors subserved by vagal afferents exert a tonic inhibitory influence on the vasomotor neurons controlling the efferent sympathetic discharge to muscle and renal resistance vessels. However, Mancia and Donald 25 demonstrated in dogs with constant flow extracorporeal circulation, in which changes in aortic pressure reflect changes in TPR, that inhibition of the cardiopulmonary receptors induces changes in arterial pressure.…”

Section: Discussioncontrasting

confidence: 51%

Impaired control of vasopressin release in hypertensive subjects with cardiac hypertrophy.

et al. 1987

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SUMMARY The effects of graded lower body negative pressure (-10 and -40 mm Hg) on vascular resistance and plasma vasopressin, norepinephrine, and renin activity were assessed in seven hypertensive subjects with left ventricular hypertrophy and seven sex-matched and age-matched normotensive subjects. In both groups increasing levels of lower body negative pressure induced a progressive decrease in right atrial pressure and an increase in vascular resistance. In normal subjects plasma vasopressin, norepinephrine, and renin activity were progressively raised, whereas only the higher level of stimulation increased plasma renin activity, norepinephrine, and vasopressin in hypertensive subjects. Propranolol induced a significant increase in plasma vasopressin in normal subjects (from 1.3 ± 0.1 to 2.0 ± 0.1 pg/ml; p<0.05) but not in hypertensive subjects. In this latter condition -10 mm Hg lower body negative pressure failed to increase plasma vasopressin, norepinephrine, and renin activity in normal subjects. Propranolol abolished the change in plasma renin activity in both groups, reduced the increase in vascular resistance induced by -40 mm Hg lower body negative pressure in normotensive subjects, but did not modify the rise in vasopressin elicited by this stimulus in normal subjects or the humoral and hemodynamic reflex responses evoked in hypertensive subjects. These results suggest that cardiopulmonary receptors are involved in the control of vasopressin release in normal subjects, whereas in hypertensive subjects with left ventricular hypertrophy, this control is altered because of an impaired function of cardiopulmonary receptors. (Hypertension 10: 595-602, 1987) KEY WORDS • propranolol • lower body negative pressure • norepinephrine A LTHOUGH the sensitivity of the nonosmotic / \ control of arginine vasopressin (AVP) release A. JL. in humans seems to be somewhat controversial, 1 " 4 recent reports 5 ' 6 support the hypothesis that factors other than blood osmolarity are involved in the regulation of AVP release in humans. In particular, Leimbach et al. 5 demonstrated that combined unloading of cardiac and arterial baroreceptors induced by lower body negative pressure (LBNP) increases plasma AVP in subjects with high plasma osmolality. Egan et al. 6 reported that the selective unloading of cardiopulmonary receptors, by thigh-cuff inflation, increases plasma AVP levels in humans. These observations raise the possibility that AVP release may be altered in patients with impaired cardiopulmonary or arterial baroreceptor reflex responsiveness.From the Istituto di Clinica Medica I, II Facolta di Medicina e Chirurgia, Universita di Napoli, Italy.Address for reprints: Bruno Trimarco, M.D., Istituto di Clinica Medica I, II Facolta di Medicina, via S. Pansini 5, 80131 Napoli, Italy.Received November 4, 1986; accepted June 30, 1987. In patients with established hypertension, we observed that the postural change from the supine to the upright position did not induce the rise in AVP plasma levels observed in normote...

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Section: Discussioncontrasting

confidence: 51%

Impaired control of vasopressin release in hypertensive subjects with cardiac hypertrophy.

et al. 1987

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“…Finally, in the cat, activation of myelinated cardiac vagal afferents at high frequencies and in the absence of the arterial baroreceptors has been shown to have only weak cardioaccelerator and vasopressor effects, whereas activation of both myelinated and nonmyelinated cardiac vagal afferents resulted in profound bradycardia and hypotension in spite of functioning arterial baroreceptors. 22 Although we have no way of completely excluding activation of excitatory receptors which might account for the observed differences, in view of our postvagotomy data and the other evidence cited above, it is unlikely that the differential responses can be explained on the basis of activation of excitatory receptors during LAD occlusion.…”

Section: Figure 4 Changes In Gracilis Perfusion Pressure During Circumentioning

confidence: 62%

Preferential distribution of inhibitory cardiac receptors with vagal afferents to the inferoposterior wall of the left ventricle activated during coronary occlusion in the dog.

Thames¹,

Klopfenstein²,

Abboud³

et al. 1978

Circulation Research

197

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The purpose of this study was to determine the relative magnitudes of the reflex effects mediated by cardiac receptors during anterior as opposed to inferoposterior ischemia of the left ventricle of the dog. Cessation of perfusion (coronary "occlusion") of the circumflex coronary artery (Cx) in 29 chloralose-anesthetized dogs with common carotids ligated (group I) resulted in significant bradycardia and hypotension, but in no significant change in perfusion pressure in the gracilis muscle perfused at constant flow. Occlusion of the left anterior descending coronary artery (LAD) produced less hypotension, no change in heart rate, and vasoconstriction in the gracilis. After vagotomy and aortic nerve section, no significant change in heart rate or gracilis perfusion pressure was observed during lad or Cx occlusion, and the blood pressure responses to LAD and Cx occlusion were not different. In nine dogs with sinoaortic denervation (group II), brief Cx occlusion resulted in bradycardia, hypotension, and vasodilation in the gracilis muscle. LAD occlusion in group II dogs caused less hypotension and no change in heart rate or gracilis perfusion pressure. After vagotomy, the bradycardia and vasodilation resulting from Cx occlusion were abolished and the blood pressure responses to LAD and Cx occlusion were not different. The weights of left ventricle perfused by each occluded vessel were not different. These data show that left ventricular receptors with vagal afferents which are activated during coronary occlusion and which mediate cardioinhibitory and vasodepressor responses are located mainly in the inferoposterior left ventricle of the dog heart.

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“…We did not investigate the possibility of their containing fibres controlling mucus secretion, although one would expect these to travel with the corresponding motor supply. (Oberg & Thoren, 1973 Mitchell & Warwick, 1955). Some of the disagreement may be due to genuine species differences, but this still would not explain different results on the same species.…”

Section: Discussionmentioning

confidence: 98%

The location of cardiac vagal preganglionic motoneurones in the medulla of the cat.

McAllen¹,

Spyer²

1976

The Journal of Physiology

222

100

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SUMMARY1. Electrophysiological techniques have been used to locate the origin of preganglionic vagal motoneurones supplying the heart of the cat.2. The right cardiac vagal branches were identified anatomically and their ability to slow the heart was assessed by electrical stimulation. Control -experiments revealed that contamination of cardiac branches by bronchomotor and oesophageal efferent fibres was likely to be small.3. Fifty-seven neurones in the medulla were activated antidromically on stimulating the cardiac branches at up to 5 times the threshold for cardiac slowing. They had axons with conduction velocities between 3 and 15 m/sec, corresponding to B fibres.4. None of these were located in the region of the dorsal motor nucleus of the vagus, in spite of repeated sampling there, but all were located in the region of the nucleus ambiguus. Histological examination of marked neurones (forty-six of the fifty-seven neurones) revealed that they were associated with its principal column, rostral to the obex.5. Sampling motoneurones of the dorsal motor nucleus revealed that most sent axons down the thoracic vagus below the cardiac branches.

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Circulatory Responses to Stimulation of Medullated and Non‐medullated Afferents in the Cardiac Nerve in the Cat

Abstract: OBERG, B. and P. T H O R~N .Circulatory responses to stimulation of medullatcd and non-medullated afferents in the cardiac nerve in the cat. Acta physiol. scand.

Cited by 89 publications

References 25 publications

Impaired control of vasopressin release in hypertensive subjects with cardiac hypertrophy.

Impaired control of vasopressin release in hypertensive subjects with cardiac hypertrophy.

Preferential distribution of inhibitory cardiac receptors with vagal afferents to the inferoposterior wall of the left ventricle activated during coronary occlusion in the dog.

The location of cardiac vagal preganglionic motoneurones in the medulla of the cat.

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