A central mechanism of acute baroreflex resetting in the conscious dog

W. Tan, M. J. Panzenbeck, M. A. Hajdu, Irving H Zucker

Research output: Contribution to journalArticle

12 Citations (Scopus)

Abstract

The role of the central nervous system in the mechanism(s) involved in acute carotid baroreflex resetting was studied in six conscious, chronically instrumented, aortic-denervated dogs. Dogs were prepared for reversible vascular isolation of the carotid sinuses. Acute baroreflex resetting was induced by holding the left carotid sinus pressure (LC(csp)) at a given value for 20 minutes using a pulsatile pressure control system while at the same time keeping the right carotid sinus pressure (RCSP) at a subthreshold level (approximately 40 mm Hg). At the end of the 20 minutes, the LC(csp) was reduced to approximately 20 mm Hg, and a baroreflex (RCSP-mean arterial pressure [MAP]) curve was generated on the right carotid sinus using static-step increases in carotid sinus pressure. At the control LC(csp) of 100 mm Hg, the RCSP-MAP baroreflex had a threshold pressure (P(th)) of 86.6 ± 3.1 mm Hg and a set point pressure (Psp) of 104.7 ± 2.5 mm Hg. Increasing LC(csp) to 140 mm Hg for 20 minutes caused these parameters for the right carotid baroreflex to increase. P(th) and Psp increased by 18.4 ± 4.0 and 14.2 ± 3.0 mm Hg, respectively (p < 0.05). The baroreflex curve, therefore, was shifted upward and to the right. Decreasing LC(csp) to 60 mm Hg caused P(th) and Psp to decrease by 24.7 ± 5.0 and 18.1 ± 2 mm Hg, respectively (p < 0.05). The baroreflex curve was therefore shifted downward and to the left. The percent of resetting of P(th) and Psp was 46 ± 9% and 36 ± 8%, respectively, when LC(csp) was 140 mm Hg. These values were 61 ± 14% and 46 ± 5%, respectively, when the LC(csp) was set to 60 mm Hg. These results show that conditioning of the ipsilateral carotid sinus baroreceptors can induce acute baroreflex resetting from the contralateral, unconditioned carotid sinus. This strongly suggests that the conditioning pressure can cause baroreflex resetting by a central mechanism alone wihout the need for the receptors themselves to be reset.

Original languageEnglish (US)
Pages (from-to)63-70
Number of pages8
JournalCirculation Research
Volume65
Issue number1
DOIs
StatePublished - Jan 1 1989

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Carotid Sinus
Baroreflex
Dogs
Pressure
Arterial Pressure
Pressoreceptors

ASJC Scopus subject areas

  • Physiology
  • Cardiology and Cardiovascular Medicine

Cite this

A central mechanism of acute baroreflex resetting in the conscious dog. / Tan, W.; Panzenbeck, M. J.; Hajdu, M. A.; Zucker, Irving H.

In: Circulation Research, Vol. 65, No. 1, 01.01.1989, p. 63-70.

Research output: Contribution to journalArticle

Tan, W. ; Panzenbeck, M. J. ; Hajdu, M. A. ; Zucker, Irving H. / A central mechanism of acute baroreflex resetting in the conscious dog. In: Circulation Research. 1989 ; Vol. 65, No. 1. pp. 63-70.
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abstract = "The role of the central nervous system in the mechanism(s) involved in acute carotid baroreflex resetting was studied in six conscious, chronically instrumented, aortic-denervated dogs. Dogs were prepared for reversible vascular isolation of the carotid sinuses. Acute baroreflex resetting was induced by holding the left carotid sinus pressure (LC(csp)) at a given value for 20 minutes using a pulsatile pressure control system while at the same time keeping the right carotid sinus pressure (RCSP) at a subthreshold level (approximately 40 mm Hg). At the end of the 20 minutes, the LC(csp) was reduced to approximately 20 mm Hg, and a baroreflex (RCSP-mean arterial pressure [MAP]) curve was generated on the right carotid sinus using static-step increases in carotid sinus pressure. At the control LC(csp) of 100 mm Hg, the RCSP-MAP baroreflex had a threshold pressure (P(th)) of 86.6 ± 3.1 mm Hg and a set point pressure (Psp) of 104.7 ± 2.5 mm Hg. Increasing LC(csp) to 140 mm Hg for 20 minutes caused these parameters for the right carotid baroreflex to increase. P(th) and Psp increased by 18.4 ± 4.0 and 14.2 ± 3.0 mm Hg, respectively (p < 0.05). The baroreflex curve, therefore, was shifted upward and to the right. Decreasing LC(csp) to 60 mm Hg caused P(th) and Psp to decrease by 24.7 ± 5.0 and 18.1 ± 2 mm Hg, respectively (p < 0.05). The baroreflex curve was therefore shifted downward and to the left. The percent of resetting of P(th) and Psp was 46 ± 9{\%} and 36 ± 8{\%}, respectively, when LC(csp) was 140 mm Hg. These values were 61 ± 14{\%} and 46 ± 5{\%}, respectively, when the LC(csp) was set to 60 mm Hg. These results show that conditioning of the ipsilateral carotid sinus baroreceptors can induce acute baroreflex resetting from the contralateral, unconditioned carotid sinus. This strongly suggests that the conditioning pressure can cause baroreflex resetting by a central mechanism alone wihout the need for the receptors themselves to be reset.",
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