- Title
- Central nervous μ-opioid and 5-hydroxytryptamine influence on baroreflex evoked coronary vasodilatation in the dog
- Creator
- White, Saxon William; Gazibarich, G. J.; Porges, W. L.; Moore, P. G.
- Relation
- Blood Vessels Vol. 23, Issue 2
- Publisher Link
- http://dx.doi.org/10.1159/000158626
- Publisher
- S. Karger AG
- Resource Type
- journal article
- Date
- 1986
- Description
- Stimulation of arterial baroreceptors caused coronary vasodilatation by vagal activation and reciprocal withdrawal of sympathetic tone. The influence of central nervous μ-opioid/5-hydroxytryptamine (5-HT) interactions in the central nervous system on baroreflex control of circumflex conductance (CC; Doppler flowmeter) was studied in unsedated dogs (in heart block with paced ventricles) at rest and during acute rises in aortic pressure (AP; balloon inflation in thoracic aorta). Fentanyl (a μ-opioid receptor agonist anesthetic agent used in man) was infused intravenously at 0.551μg kg⁻¹ min⁻¹; dogs were studied before and I week after intracisternal injection of 610 μg kg⁻¹ 5,7-dihydroxytryptamine (5,7-DHT) to deplete 5-HT in the central nervous system. Fentanyl infusion beyond 10 min caused a progressive rise in AP and a fall in CC, effects blocked by naloxone. The gain (=%ΔCC:%ΔAP) of the baroreflex dilator response was enhanced to 150% of resting. One week after intracisternal 5,7-DHT gain of the baroreflex was diminished. When fentanyl was infused, no consistent changes in AP and CC were observed, but all dogs showed recovery or gain (average to 172%) or the coronary vasodilator reflex. These data suggest that μ-opioid receptor mechanisms in the central nervous system enhance gain of the vagal component of the coronary reflex through 5 HT independent mechanisms.
- Subject
- coronary vasodilatation; central nervous system; baroreflex control; circumflex conductance
- Identifier
- http://hdl.handle.net/1959.13/939158
- Identifier
- uon:12746
- Identifier
- ISSN:0303-6847
- Language
- eng
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