| Role of parabrachial nucleus in baroreflex-mediated coronary vasoconstriction. | |
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MedLine Citation:
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PMID: 8853344 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Coronary vasoconstriction is a component of the baroreflex response to bilateral carotid occlusion. The central pathways responsible for this reflex constriction are incompletely understood, but previous studies show that activation of parabrachial nucleus (PBN) elicits coronary vasoconstriction and that PBN shares prominent anatomic connections with other central baroreflex centers, including the nucleus of the tractus solitarius. Therefore, we examined whether PBN plays a role in baroreflex mediated coronary constriction and whether cell bodies rather than fibers passing through this region are involved. Anesthetized cats were instrumented for continuous measurements of heart rate, arterial pressure, and coronary flow velocity. Bilateral carotid occlusion following propranolol and vagotomy increased arterial pressure (63 +/- 10%) and an index of coronary vascular resistance (34 +/- 6%). Bilateral microinjections of lidocaine (1%, 400 nl) into PBN reversibly attenuated the coronary constriction (19 +/- 5%) with little effect on the change in arterial pressure. It was further demonstrated that autoregulatory responses to the increase in pressure could not fully account for the observed changes in coronary constriction. In a separate group of animals, kainic acid (50 mM, 300 nl) abolished the baroreflex increase in coronary resistance (43 +/- 1 vs. -9 +/- 9% after) without affecting the increase in arterial pressure (54 +/- 12% increase before vs. 55 +/- 20% increase after kainic acid). We conclude that PBN is a necessary component of the baroreflex pathway mediating coronary vasoconstriction. Furthermore, cell bodies in PBN, rather than simply fibers passing through that region, participate in the reflex coronary vasoconstriction. |
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Authors:
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D D Gutterman; A Goodson |
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Publication Detail:
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Type: Journal Article |
Journal Detail:
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Title: The American journal of physiology Volume: 271 ISSN: 0002-9513 ISO Abbreviation: Am. J. Physiol. Publication Date: 1996 Sep |
Date Detail:
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Created Date: 1996-12-05 Completed Date: 1996-12-05 Revised Date: 2003-11-14 |
Medline Journal Info:
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Nlm Unique ID: 0370511 Medline TA: Am J Physiol Country: UNITED STATES |
Other Details:
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Languages: eng Pagination: H1079-86 Citation Subset: IM |
Affiliation:
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Veterans Administration Medical Center, Iowa City 52246-2208, USA. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Animals Arterial Occlusive Diseases / physiopathology Baroreflex / physiology* Blood Pressure / drug effects, physiology Carotid Artery Diseases / physiopathology Cats Coronary Circulation / drug effects, physiology* Kainic Acid / pharmacology Lidocaine / pharmacology Pons / physiology* Propranolol / pharmacology Vagotomy Vascular Resistance / drug effects, physiology Vasoconstriction / drug effects, physiology* Vasodilator Agents / pharmacology |
| Chemical | |
Reg. No./Substance:
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0/Vasodilator Agents; 137-58-6/Lidocaine; 487-79-6/Kainic Acid; 525-66-6/Propranolol |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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