α- and β-adrenergic mechanisms in the control of vascular capacitance by the carotid sinus baroreflex system

K. Shigemi, M. J. Brunner, Artin A Shoukas

Research output: Contribution to journalArticle

Abstract

We examined the active and passive contributions of the α- and β- adrenergic receptor mechanisms to the changes in systemic vascular capacitance caused by the carotid sinus baroreflex system in anesthetized, vagotomized dogs. The carotid sinuses were isolated from the systemic circulation and perfused with controlled pressures. To determine the changes in vascular capacitance, a constant flow, constant venous pressure cardiopulmonary bypass was used. The changes in unstressed vascular volume were calculated when carotid sinus pressure was reduced from 200 to 50 mmHg without any adrenergic receptor antagonist, with either an α- (phentolamine) or a β- (propranolol) antagonist and then with both. The reflex change in unstressed vascular volume in the systemic circulation (22.6 ± 9.0 ml/kg without any antagonist) was reduced by 72% with phentolamine, by 35% with propranolol, and by 73% with both antagonists. Our results suggest that the α-adrenergic mechanisms contribute significantly to active changes in systemic venous capacity. In addition, the β-adrenergic system has very little effect on active changes in venous vessels but does contribute to the overall capacity changes by dilating the hepatic outflow resistance when the carotid sinus baroreflex system is activated.

Original languageEnglish (US)
JournalAmerican Journal of Physiology - Heart and Circulatory Physiology
Volume267
Issue number1 36-1
StatePublished - 1994

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Vascular Capacitance
Carotid Sinus
capacitance
Baroreflex
sinuses
blood vessels
Adrenergic Agents
antagonists
propranolol
Phentolamine
adrenergic receptors
Propranolol
Blood Vessels
Pressure
Adrenergic Antagonists
Venous Pressure
Cardiopulmonary Bypass
reflexes
Adrenergic Receptors
Reflex

Keywords

  • baroreceptors
  • hepatic resistance
  • phentolamine
  • pressoreceptors
  • propranolol
  • unstressed vascular volume
  • vascular capacity
  • vascular resistance

ASJC Scopus subject areas

  • Physiology
  • Agricultural and Biological Sciences(all)

Cite this

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title = "α- and β-adrenergic mechanisms in the control of vascular capacitance by the carotid sinus baroreflex system",
abstract = "We examined the active and passive contributions of the α- and β- adrenergic receptor mechanisms to the changes in systemic vascular capacitance caused by the carotid sinus baroreflex system in anesthetized, vagotomized dogs. The carotid sinuses were isolated from the systemic circulation and perfused with controlled pressures. To determine the changes in vascular capacitance, a constant flow, constant venous pressure cardiopulmonary bypass was used. The changes in unstressed vascular volume were calculated when carotid sinus pressure was reduced from 200 to 50 mmHg without any adrenergic receptor antagonist, with either an α- (phentolamine) or a β- (propranolol) antagonist and then with both. The reflex change in unstressed vascular volume in the systemic circulation (22.6 ± 9.0 ml/kg without any antagonist) was reduced by 72{\%} with phentolamine, by 35{\%} with propranolol, and by 73{\%} with both antagonists. Our results suggest that the α-adrenergic mechanisms contribute significantly to active changes in systemic venous capacity. In addition, the β-adrenergic system has very little effect on active changes in venous vessels but does contribute to the overall capacity changes by dilating the hepatic outflow resistance when the carotid sinus baroreflex system is activated.",
keywords = "baroreceptors, hepatic resistance, phentolamine, pressoreceptors, propranolol, unstressed vascular volume, vascular capacity, vascular resistance",
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AU - Shigemi, K.

AU - Brunner, M. J.

AU - Shoukas, Artin A

PY - 1994

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N2 - We examined the active and passive contributions of the α- and β- adrenergic receptor mechanisms to the changes in systemic vascular capacitance caused by the carotid sinus baroreflex system in anesthetized, vagotomized dogs. The carotid sinuses were isolated from the systemic circulation and perfused with controlled pressures. To determine the changes in vascular capacitance, a constant flow, constant venous pressure cardiopulmonary bypass was used. The changes in unstressed vascular volume were calculated when carotid sinus pressure was reduced from 200 to 50 mmHg without any adrenergic receptor antagonist, with either an α- (phentolamine) or a β- (propranolol) antagonist and then with both. The reflex change in unstressed vascular volume in the systemic circulation (22.6 ± 9.0 ml/kg without any antagonist) was reduced by 72% with phentolamine, by 35% with propranolol, and by 73% with both antagonists. Our results suggest that the α-adrenergic mechanisms contribute significantly to active changes in systemic venous capacity. In addition, the β-adrenergic system has very little effect on active changes in venous vessels but does contribute to the overall capacity changes by dilating the hepatic outflow resistance when the carotid sinus baroreflex system is activated.

AB - We examined the active and passive contributions of the α- and β- adrenergic receptor mechanisms to the changes in systemic vascular capacitance caused by the carotid sinus baroreflex system in anesthetized, vagotomized dogs. The carotid sinuses were isolated from the systemic circulation and perfused with controlled pressures. To determine the changes in vascular capacitance, a constant flow, constant venous pressure cardiopulmonary bypass was used. The changes in unstressed vascular volume were calculated when carotid sinus pressure was reduced from 200 to 50 mmHg without any adrenergic receptor antagonist, with either an α- (phentolamine) or a β- (propranolol) antagonist and then with both. The reflex change in unstressed vascular volume in the systemic circulation (22.6 ± 9.0 ml/kg without any antagonist) was reduced by 72% with phentolamine, by 35% with propranolol, and by 73% with both antagonists. Our results suggest that the α-adrenergic mechanisms contribute significantly to active changes in systemic venous capacity. In addition, the β-adrenergic system has very little effect on active changes in venous vessels but does contribute to the overall capacity changes by dilating the hepatic outflow resistance when the carotid sinus baroreflex system is activated.

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KW - vascular resistance

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