Inhibition of adrenergic outflow to peripheral blood vessels by vagal afferents from the cardiopulmonary region in the dog

G. Mancia, D. E. Donald, J. T. Shepherd

Research output: Contribution to journalArticle

51 Citations (Scopus)

Abstract

In closed chest atropinized dogs anesthetized with chloralose and ventilated artificially, the aortic nerves were cut beneath the nodose ganglion, and the carotid sinuses were either denervated or vascularly isolated and maintained at a pressure of 40 mm Hg. Denervation was established by the failure of the pressoreceptor systems to respond to mechanical stimulation. Cold block or section of the cervical vagi resulted in statistically significant increases in arterial blood pressure (18%), heart rate (3%), central venous pressure (13%), hind limb perfusion pressure (12%), pressure within the occluded spleen (18%), and efferent renal sympathetic nerve activity (28%). There was no change in saphenous vein perfusion pressure. The vascular responses were abolished by α receptor blockade and were not affected by section of the vagi at the diaphragm. When the pressure in the vascularly isolated innervated carotid sinuses was varied from 40 to 220 mm Hg, the vascular responses to vagal block decreased steeply between 100 and 160 mm Hg and were absent at 200 mm Hg. Thus, receptors in the cardiopulmonary region with afferent vagal fibers exert a continuous restraint on the sympathetic adrenergic outflow to resistance and capacitance vessels, especially when the input from the carotid baroreceptors is decreased.

Original languageEnglish
Pages (from-to)713-721
Number of pages9
JournalCirculation Research
Volume33
Issue number6
Publication statusPublished - 1973

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Adrenergic Agents
Blood Vessels
Dogs
Pressure
Carotid Sinus
Pressoreceptors
Perfusion
Nodose Ganglion
Chloralose
Central Venous Pressure
Saphenous Vein
Denervation
Diaphragm
Arterial Pressure
Thorax
Spleen
Extremities
Heart Rate
Kidney

ASJC Scopus subject areas

  • Physiology
  • Cardiology and Cardiovascular Medicine

Cite this

Inhibition of adrenergic outflow to peripheral blood vessels by vagal afferents from the cardiopulmonary region in the dog. / Mancia, G.; Donald, D. E.; Shepherd, J. T.

In: Circulation Research, Vol. 33, No. 6, 1973, p. 713-721.

Research output: Contribution to journalArticle

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AB - In closed chest atropinized dogs anesthetized with chloralose and ventilated artificially, the aortic nerves were cut beneath the nodose ganglion, and the carotid sinuses were either denervated or vascularly isolated and maintained at a pressure of 40 mm Hg. Denervation was established by the failure of the pressoreceptor systems to respond to mechanical stimulation. Cold block or section of the cervical vagi resulted in statistically significant increases in arterial blood pressure (18%), heart rate (3%), central venous pressure (13%), hind limb perfusion pressure (12%), pressure within the occluded spleen (18%), and efferent renal sympathetic nerve activity (28%). There was no change in saphenous vein perfusion pressure. The vascular responses were abolished by α receptor blockade and were not affected by section of the vagi at the diaphragm. When the pressure in the vascularly isolated innervated carotid sinuses was varied from 40 to 220 mm Hg, the vascular responses to vagal block decreased steeply between 100 and 160 mm Hg and were absent at 200 mm Hg. Thus, receptors in the cardiopulmonary region with afferent vagal fibers exert a continuous restraint on the sympathetic adrenergic outflow to resistance and capacitance vessels, especially when the input from the carotid baroreceptors is decreased.

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