Journal article
Coronary Vascular Responses to Stimulation of Chemoreceptors and Baroreceptors: EVIDENCE FOR REFLEX ACTIVATION OF VAGAL CHOLINERGIC INNERVATION
Circulation research, Vol.31(1), pp.8-17
07/1972
DOI: 10.1161/01.RES.31.1.8
PMID: 4402639
Abstract
Coronary vascular responses to stimulation of chemoreceptors were studied in anesthetized, artificially ventilated dogs. The circumflex coronary artery was perfused at constant flow so that changes in perfusion pressure reflected changes in coronary resistance. Practolol, a myocardioselective beta-receptor antagonist, and pacing were used to minimize indirect effects of myocardial responses on coronary resistance. Carotid and aortic injections of nicotine produced decreases in coronary perfusion pressure averaging -21 mm Hg and -22 mm Hg, respectively. Decreases with carotid and aortic injections of cyanide averaged -8 mm Hg and -17 mm Hg, respectively. These coronary dilator responses were abolished by bilateral vagotomy or atropine. Changes in perfusion pressure with carotid injections of nicotine averaged +3 mm Hg after vagotomy and +2 mm Hg after administration of atropine. The coronary dilator responses to carotid chemoreceptor stimulation were accompanied by increases in coronary sinus Po2 in five studies and no change in two studies. Carotid sinus nerve stimulation caused abrupt and sustained coronary vasodilatation. After vagotomy or administration of atropine, the response to carotid sinus nerve stimulation was no longer abrupt but occurred gradually, suggesting that a component of the reflex response was blocked. These studies indicate that stimulation of chemoreceptors activates a vagal cholinergic vasodilator pathway to coronary vessels in the dog. Activation of this pathway appears also to contribute to reflex coronary responses to stimulation of baroreceptors.
Details
- Title: Subtitle
- Coronary Vascular Responses to Stimulation of Chemoreceptors and Baroreceptors: EVIDENCE FOR REFLEX ACTIVATION OF VAGAL CHOLINERGIC INNERVATION
- Creators
- James G Hackett - Cardiovascular Division, Department of Internal Medicine, University of Iowa College of Medicine, and the Veterans Administration Hospital Iowa City, Iowa 52240Francois M Abboud - Cardiovascular Division, Department of Internal Medicine, University of Iowa College of Medicine, and the Veterans Administration Hospital Iowa City, Iowa 52240Allyn L Mark - Cardiovascular Division, Department of Internal Medicine, University of Iowa College of Medicine, and the Veterans Administration Hospital Iowa City, Iowa 52240Phillip G Schmid - Cardiovascular Division, Department of Internal Medicine, University of Iowa College of Medicine, and the Veterans Administration Hospital Iowa City, Iowa 52240Donald D Heistad - Cardiovascular Division, Department of Internal Medicine, University of Iowa College of Medicine, and the Veterans Administration Hospital Iowa City, Iowa 52240Dennis Bollard - Cardiovascular Division, Department of Internal Medicine, University of Iowa College of Medicine, and the Veterans Administration Hospital Iowa City, Iowa 52240Leonard Brooks - Cardiovascular Division, Department of Internal Medicine, University of Iowa College of Medicine, and the Veterans Administration Hospital Iowa City, Iowa 52240
- Resource Type
- Journal article
- Publication Details
- Circulation research, Vol.31(1), pp.8-17
- DOI
- 10.1161/01.RES.31.1.8
- PMID
- 4402639
- ISSN
- 0009-7330
- eISSN
- 1524-4571
- Language
- English
- Date published
- 07/1972
- Academic Unit
- Molecular Physiology and Biophysics; Cardiovascular Medicine; Fraternal Order of Eagles Diabetes Research Center; Neuroscience and Pharmacology; Cardiothoracic Surgery; Internal Medicine
- Record Identifier
- 9984025687002771
Metrics
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