Widespread neural excitation initiated from cardiac spinal afferent nerves

L. C. Weaver, R. L. Meckler, H. K. Fry and S. Donoghue Reflex effects of cardiac sympathetic afferent nerve excitation on cardiac and renal components of sympathetic outflow have been well investigated, but the extent of these cardiac afferent influences on other sympathetic nerves or on respiratory...

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Veröffentlicht in:American journal of physiology. Regulatory, integrative and comparative physiology integrative and comparative physiology, 1983-08, Vol.245 (2), p.241-R250
Hauptverfasser: Weaver, L. C, Meckler, R. L, Fry, H. K, Donoghue, S
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Sprache:eng
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Zusammenfassung:L. C. Weaver, R. L. Meckler, H. K. Fry and S. Donoghue Reflex effects of cardiac sympathetic afferent nerve excitation on cardiac and renal components of sympathetic outflow have been well investigated, but the extent of these cardiac afferent influences on other sympathetic nerves or on respiratory or cortical neural systems is unknown. Therefore such influences were investigated electrophysiologically in anesthetized, vagotomized, baroreceptor-denervated cats. Stimulation of cardiac sympathetic spinal afferent neurons by the noxious substance bradykinin caused excitation of cardiac, renal, splenic, gastrohepatic, adrenal, and deep peroneal (muscle) vasoconstrictor sympathetic nerves, as well as excitation of phrenic nerves and concomitant desynchronization of the electroencephalogram. Possible supraspinal pathways mediating these responses were investigated. Sympathetic reflexes caused by cardiac afferent stimulation were unchanged after decerebration, thereby demonstrating that supramedullary mediation was not essential to the sympathetic responses. Potential contributions of the medulla to the observed sympathetic or other responses were demonstrated by recording from medullary neurons responsive to electrical and chemical stimulation of the afferent nerves. In summary, noxious stimulation of cardiac sympathetic afferent neurons leads to widespread neural excitation which may contribute to sensory, visceral, and somatic responses caused by cardiac pain or which occur during activated states such as exercise or emotional stress.
ISSN:0363-6119
0002-9513
1522-1490
DOI:10.1152/ajpregu.1983.245.2.R241