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Ferguson AV, Smith P. Autonomic mechanisms underlying area postrema stimulation-induced cardiovascular responses in rats. Am J Physiol. 1991;261(1):R1-8doi: 10.1152/ajpregu.1991.261.1.R1.
Ferguson, A. V., & Smith, P. (1991). Autonomic mechanisms underlying area postrema stimulation-induced cardiovascular responses in rats. The American journal of physiology, 261(1), R1-8. https://doi.org/10.1152/ajpregu.1991.261.1.R1
Ferguson, A V, and Smith, P. "Autonomic mechanisms underlying area postrema stimulation-induced cardiovascular responses in rats." The American journal of physiology vol. 261,1 (1991): R1-8. doi: https://doi.org/10.1152/ajpregu.1991.261.1.R1
Ferguson AV, Smith P. Autonomic mechanisms underlying area postrema stimulation-induced cardiovascular responses in rats. Am J Physiol. 1991 Jul;261(1):R1-8. doi: 10.1152/ajpregu.1991.261.1.R1. PMID: 1677538.
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Am J Physiol. 1991 Jul;261(1):R1-8. doi: 10.1152/ajpregu.1991.261.1.R1.

Autonomic mechanisms underlying area postrema stimulation-induced cardiovascular responses in rats.

The American journal of physiology

A V Ferguson, P Smith

Affiliations

  1. Department of Physiology, Queen's University, Kingston, Ontario, Canada.

PMID: 1677538 DOI: 10.1152/ajpregu.1991.261.1.R1

Abstract

Experiments were designed to examine the autonomic mechanisms underlying the decreases in blood pressure and heart rate elicited by electrical stimulation in the rat area postrema (AP). Vagotomy was found to significantly reduce the bradycardia observed in response to AP stimulation (control -123.5 +/- 23.5 beats/min; vagotomized -7 +/- 5.4 beats/min; P less than 0.001) but was without significant effect on blood pressure responses. Hexamethonium significantly reduced both heart rate (control -225.5 +/- 11.9 beats/min; hexamethonium -5.5 +/- 2.8 beats/min; P less than 0.001) and depressor (control -35.4 +/- 4.7 mmHg; hexamethonium -6.4 +/- 0.8 mmHg; P less than 0.001) responses to such stimulation, whereas combined alpha- and beta-adrenergic blockade was without effect. The muscarinic blocking agent atropine also abolished both blood pressure (control -22.0 +/- 4.3 mmHg; atropine 2.8 +/- 4.4 mmHg; P less than 0.01) and heart rate (control -187.0 +/- 41.9 beats/min; atropine 8.8 +/- 2.6 beats/min; P less than 0.01) responses to AP stimulation. These data suggest that AP stimulation influences two separate neural pathways eliciting distinct cardiovascular responses. It would appear that activation of one of these pathways results in activation of vagal efferents to the heart and thus bradycardia. A second parallel pathway influenced by AP stimulation apparently elicits depressor response through actions on cholinergic muscarinic receptors.

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